Structured Review

Millipore chemicals cisplatin
Average 500 MHz 1 H NMR spectra of aqueous kidney extracts of BALB/c mice after 1 h of post-injection with ( a ) phosphate buffer saline solution (controls), ( b ) <t>cisplatin</t> (cDDP), and ( c ) dinuclear Pd(II) complex with spermine (Pd 2 Spm). * Cut-off spectral region due to water suppression (δ 4.53–5.20); cont.: contamination. Arrows represent noticeable metabolite variations in drug-exposed samples compared to controls. Dashed lines are used to guide the eye. Metabolite abbreviations: three-letter code used for amino acids; Acet., acetate; Ado, adenosine; ADP, adenosine diphosphate; ATP, adenosine triphosphate; Cho, choline; Cre, creatine; DMA, dimethylamine; DMSO 2 , dimethyl sulfone (tentative assignment); Glc, glucose; GPC, glycerophosphocholine; Hip, hippurate; Ino, inosine; Lac, lactate; PC, phosphocholine; Tau, taurine; TMAO, trimethylamine- N -oxide; Urd, uridine.
Chemicals Cisplatin, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Novel Insights into Mice Multi-Organ Metabolism upon Exposure to a Potential Anticancer Pd(II)-Agent"

Article Title: Novel Insights into Mice Multi-Organ Metabolism upon Exposure to a Potential Anticancer Pd(II)-Agent

Journal: Metabolites

doi: 10.3390/metabo11020114

Average 500 MHz 1 H NMR spectra of aqueous kidney extracts of BALB/c mice after 1 h of post-injection with ( a ) phosphate buffer saline solution (controls), ( b ) cisplatin (cDDP), and ( c ) dinuclear Pd(II) complex with spermine (Pd 2 Spm). * Cut-off spectral region due to water suppression (δ 4.53–5.20); cont.: contamination. Arrows represent noticeable metabolite variations in drug-exposed samples compared to controls. Dashed lines are used to guide the eye. Metabolite abbreviations: three-letter code used for amino acids; Acet., acetate; Ado, adenosine; ADP, adenosine diphosphate; ATP, adenosine triphosphate; Cho, choline; Cre, creatine; DMA, dimethylamine; DMSO 2 , dimethyl sulfone (tentative assignment); Glc, glucose; GPC, glycerophosphocholine; Hip, hippurate; Ino, inosine; Lac, lactate; PC, phosphocholine; Tau, taurine; TMAO, trimethylamine- N -oxide; Urd, uridine.
Figure Legend Snippet: Average 500 MHz 1 H NMR spectra of aqueous kidney extracts of BALB/c mice after 1 h of post-injection with ( a ) phosphate buffer saline solution (controls), ( b ) cisplatin (cDDP), and ( c ) dinuclear Pd(II) complex with spermine (Pd 2 Spm). * Cut-off spectral region due to water suppression (δ 4.53–5.20); cont.: contamination. Arrows represent noticeable metabolite variations in drug-exposed samples compared to controls. Dashed lines are used to guide the eye. Metabolite abbreviations: three-letter code used for amino acids; Acet., acetate; Ado, adenosine; ADP, adenosine diphosphate; ATP, adenosine triphosphate; Cho, choline; Cre, creatine; DMA, dimethylamine; DMSO 2 , dimethyl sulfone (tentative assignment); Glc, glucose; GPC, glycerophosphocholine; Hip, hippurate; Ino, inosine; Lac, lactate; PC, phosphocholine; Tau, taurine; TMAO, trimethylamine- N -oxide; Urd, uridine.

Techniques Used: Nuclear Magnetic Resonance, Mouse Assay, Injection, Gel Permeation Chromatography

2) Product Images from "Liposomes Co-Encapsulating Cisplatin/Mifepristone Improve the Effect on Cervical Cancer: In Vitro and In Vivo Assessment"

Article Title: Liposomes Co-Encapsulating Cisplatin/Mifepristone Improve the Effect on Cervical Cancer: In Vitro and In Vivo Assessment

Journal: Pharmaceutics

doi: 10.3390/pharmaceutics12090897

Chromatographic evaluation of the concentration of cisplatin and mifepristone in L-Cis/MF. The images show the peaks for six groups: ( A ) blank liposomes; ( B ) blank liposomes spiked with 10 µg/mL cisplatin and 25 µg/mL NiCl 2 , the internal standard (IS); ( C ) cisplatin drawn from an L-Cis/MF sample and spiked with its IS; ( D ) blank liposomes; ( E ) blank liposomes spiked with 4 µg/mL mifepristone and 4 µg/mL of promegestone (IS); ( F ) mifepristone drawn from a L-Cis/MF sample and spiked with its IS.
Figure Legend Snippet: Chromatographic evaluation of the concentration of cisplatin and mifepristone in L-Cis/MF. The images show the peaks for six groups: ( A ) blank liposomes; ( B ) blank liposomes spiked with 10 µg/mL cisplatin and 25 µg/mL NiCl 2 , the internal standard (IS); ( C ) cisplatin drawn from an L-Cis/MF sample and spiked with its IS; ( D ) blank liposomes; ( E ) blank liposomes spiked with 4 µg/mL mifepristone and 4 µg/mL of promegestone (IS); ( F ) mifepristone drawn from a L-Cis/MF sample and spiked with its IS.

Techniques Used: Concentration Assay

Following the encapsulation of cisplatin and mifepristone in the liposomes, the physicochemical characterization of L-Cis/MF was carried out by measuring: ( A ) the phospholipid concentration in the fractions derived from the liposomes; ( B ) non-encapsulated mifepristone extracted from fractions 11–33; ( C ) the percentage of cisplatin (black circles) and mifepristone (black squares) released from the formulation during 96 h of incubation at room temperature. Data are expressed as the mean ± SD ( n = 3).
Figure Legend Snippet: Following the encapsulation of cisplatin and mifepristone in the liposomes, the physicochemical characterization of L-Cis/MF was carried out by measuring: ( A ) the phospholipid concentration in the fractions derived from the liposomes; ( B ) non-encapsulated mifepristone extracted from fractions 11–33; ( C ) the percentage of cisplatin (black circles) and mifepristone (black squares) released from the formulation during 96 h of incubation at room temperature. Data are expressed as the mean ± SD ( n = 3).

Techniques Used: Concentration Assay, Derivative Assay, Incubation

( A ) Efficacy of the distinct treatments on mice with HeLa cell xenografts: non-encapsulated drugs (cisplatin, mifepristone and the combination of Cis/MF), drug-loaded liposomes (L-Cis and L-Cis/MF), and the corresponding controls: no treatment (control) and empty liposomes (L-Control). HeLa cells were implanted s.c. in the flank of nude mice. The treatments were initiated when the tumors reached 150 mm 3 (day 0). ( B ) Final body weight of mice in the different groups. Data are expressed as the mean ± standard error of the mean (SEM) of 5 animals per group.
Figure Legend Snippet: ( A ) Efficacy of the distinct treatments on mice with HeLa cell xenografts: non-encapsulated drugs (cisplatin, mifepristone and the combination of Cis/MF), drug-loaded liposomes (L-Cis and L-Cis/MF), and the corresponding controls: no treatment (control) and empty liposomes (L-Control). HeLa cells were implanted s.c. in the flank of nude mice. The treatments were initiated when the tumors reached 150 mm 3 (day 0). ( B ) Final body weight of mice in the different groups. Data are expressed as the mean ± standard error of the mean (SEM) of 5 animals per group.

Techniques Used: Mouse Assay

Viability of HeLa cells during the treatments with free cisplatin (Cis), free mifepristone (MF), free cisplatin/mifepristone (Cis/MF), cisplatin-loaded liposomes (L-Cis) and cisplatin/mifepristone-loaded liposomes (L-Cis/MF). The viability assays were repeated in triplicate in at least three independent experiments. Values represent the mean ± SD.
Figure Legend Snippet: Viability of HeLa cells during the treatments with free cisplatin (Cis), free mifepristone (MF), free cisplatin/mifepristone (Cis/MF), cisplatin-loaded liposomes (L-Cis) and cisplatin/mifepristone-loaded liposomes (L-Cis/MF). The viability assays were repeated in triplicate in at least three independent experiments. Values represent the mean ± SD.

Techniques Used:

Analysis of the cell cycle for HeLa cells at days 5 and 9 post-treatment in vitro. L-Control (blank liposomes); cisplatin-loaded liposomes (L-Cis) and cisplatin/mifepristone-loaded liposomes (L-Cis/MF). Data are expressed as the mean ± SD of three independent experiments. * and # Significant difference ( p
Figure Legend Snippet: Analysis of the cell cycle for HeLa cells at days 5 and 9 post-treatment in vitro. L-Control (blank liposomes); cisplatin-loaded liposomes (L-Cis) and cisplatin/mifepristone-loaded liposomes (L-Cis/MF). Data are expressed as the mean ± SD of three independent experiments. * and # Significant difference ( p

Techniques Used: In Vitro

Analysis of apoptosis by flow cytometry in HeLa cells at day 5 post-treatment: ( A ) free cisplatin, free cisplatin/mifepristone (Cis + MF), cisplatin-loaded liposomes (L-Cis), cisplatin/mifepristone-loaded liposomes (L-Cis/MF), and empty liposomes (L-Control). * p
Figure Legend Snippet: Analysis of apoptosis by flow cytometry in HeLa cells at day 5 post-treatment: ( A ) free cisplatin, free cisplatin/mifepristone (Cis + MF), cisplatin-loaded liposomes (L-Cis), cisplatin/mifepristone-loaded liposomes (L-Cis/MF), and empty liposomes (L-Control). * p

Techniques Used: Flow Cytometry

3) Product Images from "Suppression of Cisplatin-Induced Hepatic Injury in Rats Through Alarmin High-Mobility Group Box-1 Pathway by Ganoderma lucidum: Theoretical and Experimental Study"

Article Title: Suppression of Cisplatin-Induced Hepatic Injury in Rats Through Alarmin High-Mobility Group Box-1 Pathway by Ganoderma lucidum: Theoretical and Experimental Study

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S249093

Cisplatin-induced liver injury in liver sections stained with hematoxylin-eosin. Representative microscopic pictures of liver sections showing normal histology of central vein (CV) and well organized radially arranged hepatic cords in cont group ( A and B ) and GL group ( C and D ), while disrupted organization of hepatic cords, congestion of CV, centrilobular areas of necrosis, vacuolar and hydropic degeneration in other hepatocytes ( E ). Higher magnification to show congestion (black arrow), vacuolar degeneration (red arrow) ( F ) and necrosis (arrowheads) ( G and H ) in hepatocytes of CP group. H E, ( A , C and E ) X: 100 bar 100 and ( B, D , and F – H ) X: 400 bar 50.
Figure Legend Snippet: Cisplatin-induced liver injury in liver sections stained with hematoxylin-eosin. Representative microscopic pictures of liver sections showing normal histology of central vein (CV) and well organized radially arranged hepatic cords in cont group ( A and B ) and GL group ( C and D ), while disrupted organization of hepatic cords, congestion of CV, centrilobular areas of necrosis, vacuolar and hydropic degeneration in other hepatocytes ( E ). Higher magnification to show congestion (black arrow), vacuolar degeneration (red arrow) ( F ) and necrosis (arrowheads) ( G and H ) in hepatocytes of CP group. H E, ( A , C and E ) X: 100 bar 100 and ( B, D , and F – H ) X: 400 bar 50.

Techniques Used: Staining

Hepatoprotective effect of Ganoderma lucidum on expression of caspase-3 in rat livers. (1) Representative microscopic pictures of liver sections immunostained using caspase-3 antibody showing negative staining in the control group ( A and B ) and GL group ( C and D ), while a strong positive staining as indicated by intense bright brown color in group received cisplatin ( E and F ). GLM treatment triggers moderate positive staining in i.p group ( G and H ), mild positive staining in the EOD group ( I and J ), and negative staining in the daily group ( K and L ). Black arrows point to positive staining. IHC counterstained with Mayer’s hematoxylin. X: 100 bar 100 (A, C, E, G , and I ) and X: 400 bar 50 (B, D, F, H , and J ). (2) Statistical analysis of IHC staining intensity percentages in six experimental groups showing a significant increase in caspase-3 in CP group when compared with control and GL groups, and the protective effect of GLM in different treated groups. Different small alphabetical letters means significant when P
Figure Legend Snippet: Hepatoprotective effect of Ganoderma lucidum on expression of caspase-3 in rat livers. (1) Representative microscopic pictures of liver sections immunostained using caspase-3 antibody showing negative staining in the control group ( A and B ) and GL group ( C and D ), while a strong positive staining as indicated by intense bright brown color in group received cisplatin ( E and F ). GLM treatment triggers moderate positive staining in i.p group ( G and H ), mild positive staining in the EOD group ( I and J ), and negative staining in the daily group ( K and L ). Black arrows point to positive staining. IHC counterstained with Mayer’s hematoxylin. X: 100 bar 100 (A, C, E, G , and I ) and X: 400 bar 50 (B, D, F, H , and J ). (2) Statistical analysis of IHC staining intensity percentages in six experimental groups showing a significant increase in caspase-3 in CP group when compared with control and GL groups, and the protective effect of GLM in different treated groups. Different small alphabetical letters means significant when P

Techniques Used: Expressing, Negative Staining, Staining, Immunohistochemistry

Effect of CP on fibrosis in CP-induced liver injury. Representative microscopic pictures of Masson trichrome stained liver sections, showing no collagen deposition around central vein (CV) and in portal areas (PA) scored 0 in cont group ( A and B ) and GL group ( C and D ). Meanwhile, a moderate stain ( E and F ) scored 2 to severe ( G and H ) scored 3 blue stained collagen deposition around central vein (CV) and in portal areas (PA) (black arrows) in group received cisplatin only ( E–H ). X: 100 bar 100 ( A , C , E , and G ) and X: 400 bar 50 ( B , D , F , and H ).
Figure Legend Snippet: Effect of CP on fibrosis in CP-induced liver injury. Representative microscopic pictures of Masson trichrome stained liver sections, showing no collagen deposition around central vein (CV) and in portal areas (PA) scored 0 in cont group ( A and B ) and GL group ( C and D ). Meanwhile, a moderate stain ( E and F ) scored 2 to severe ( G and H ) scored 3 blue stained collagen deposition around central vein (CV) and in portal areas (PA) (black arrows) in group received cisplatin only ( E–H ). X: 100 bar 100 ( A , C , E , and G ) and X: 400 bar 50 ( B , D , F , and H ).

Techniques Used: Staining

Summary of effects of (500 mg/kg/day) GLM in cisplatin-induced hepatotoxicity in male Sprague-Dawley rats. GLM: Ganoderma lucidum mushroom
Figure Legend Snippet: Summary of effects of (500 mg/kg/day) GLM in cisplatin-induced hepatotoxicity in male Sprague-Dawley rats. GLM: Ganoderma lucidum mushroom

Techniques Used:

4) Product Images from "Multi-Organ NMR Metabolomics to Assess In Vivo Overall Metabolic Impact of Cisplatin in Mice"

Article Title: Multi-Organ NMR Metabolomics to Assess In Vivo Overall Metabolic Impact of Cisplatin in Mice

Journal: Metabolites

doi: 10.3390/metabo9110279

Scores scatter plots from PCA (left) and PLS-DA (middle) analysis obtained for 1 H NMR spectra of ( a ) kidney, ( b ) liver, and ( c ) breast tissue of BALB/c mice at 12 h post-injection with cisplatin. LV1 loadings plots from PLS-DA analysis (right), colored according to variable importance to the projection (VIP) and with main peak assignment indicated. 3-Letter codes are used for amino acids; 3-HBA: 3-hydroxybutyrate; Ado: adenosine; ADP: adenosine monophosphate; AMP: adenosine monophosphate; ATP: adenosine monophosphate; Cho: choline; Cre: creatine; Glc: glucose; GPC: glycerophosphocholine; Ino: inosine; Lac: lactate; PC: phosphocholine; Tau: taurine.
Figure Legend Snippet: Scores scatter plots from PCA (left) and PLS-DA (middle) analysis obtained for 1 H NMR spectra of ( a ) kidney, ( b ) liver, and ( c ) breast tissue of BALB/c mice at 12 h post-injection with cisplatin. LV1 loadings plots from PLS-DA analysis (right), colored according to variable importance to the projection (VIP) and with main peak assignment indicated. 3-Letter codes are used for amino acids; 3-HBA: 3-hydroxybutyrate; Ado: adenosine; ADP: adenosine monophosphate; AMP: adenosine monophosphate; ATP: adenosine monophosphate; Cho: choline; Cre: creatine; Glc: glucose; GPC: glycerophosphocholine; Ino: inosine; Lac: lactate; PC: phosphocholine; Tau: taurine.

Techniques Used: Nuclear Magnetic Resonance, Mouse Assay, Injection, Gas Chromatography, Gel Permeation Chromatography

Heatmap illustrating the metabolic variations in ( a ) kidney, ( b ) liver, and ( c ) breast tissue of BALB/c mice at 1 h, 12 h, and 48 h post-injection with cisplatin, comparatively to the controls group. The scale is color-coded as a function of Effect Size, from minimum (dark blue) to maximum (dark red) values. Lines and columns represent metabolites and subjects, respectively. Asterisks represent the confidence interval of each variation: * p -value
Figure Legend Snippet: Heatmap illustrating the metabolic variations in ( a ) kidney, ( b ) liver, and ( c ) breast tissue of BALB/c mice at 1 h, 12 h, and 48 h post-injection with cisplatin, comparatively to the controls group. The scale is color-coded as a function of Effect Size, from minimum (dark blue) to maximum (dark red) values. Lines and columns represent metabolites and subjects, respectively. Asterisks represent the confidence interval of each variation: * p -value

Techniques Used: Mouse Assay, Injection

5) Product Images from "D-Methionine Ameliorates Cisplatin-Induced Muscle Atrophy via Inhibition of Muscle Degradation Pathway"

Article Title: D-Methionine Ameliorates Cisplatin-Induced Muscle Atrophy via Inhibition of Muscle Degradation Pathway

Journal: Integrative Cancer Therapies

doi: 10.1177/1534735419828832

Effects of d -methionine on myogenesis (myogenin and MyoD) and specific E3-ubiquitin ligase (MAFbx and MuRF-1) mRNA levels in cisplatin-induced C2C12 myotube atrophy. C2C12 myotubes were treated with Dulbecco’s modified Eagle medium (DMEM), 50 µM cisplatin or 50 µM cisplatin + 5 mM d -methionine for up to 24 hours. (A) Cellular morphological changes. (B) Real-time polymerase chain reaction. The mRNA expression levels of MAFbx, MuRF-1, myogenin, and MyoD were normalized according to the amount of β-actin. Results are representative of 3 independent experiments. Values are presented as Mean ± SD. *Indicates statistical significance when compared with the saline-treated group ( P
Figure Legend Snippet: Effects of d -methionine on myogenesis (myogenin and MyoD) and specific E3-ubiquitin ligase (MAFbx and MuRF-1) mRNA levels in cisplatin-induced C2C12 myotube atrophy. C2C12 myotubes were treated with Dulbecco’s modified Eagle medium (DMEM), 50 µM cisplatin or 50 µM cisplatin + 5 mM d -methionine for up to 24 hours. (A) Cellular morphological changes. (B) Real-time polymerase chain reaction. The mRNA expression levels of MAFbx, MuRF-1, myogenin, and MyoD were normalized according to the amount of β-actin. Results are representative of 3 independent experiments. Values are presented as Mean ± SD. *Indicates statistical significance when compared with the saline-treated group ( P

Techniques Used: Modification, Real-time Polymerase Chain Reaction, Expressing

Effects of d -methionine on gastrointestinal toxicity after cisplatin treatment. (A) Views of stomachs of the 3 groups. The dotted line borders the gastric fundus. (B) Gastric contents. (C) Quantity of gastric contents. (D) Gastric emptying index (GEI). (E) Feeding efficiency. Data are presented as mean ± SD, n = 8. Differences were analyzed by 1-way analysis of variance. The asterisk (*) indicates significant differences when compared with the saline group, and the hashtag (#) with cisplatin group ( P
Figure Legend Snippet: Effects of d -methionine on gastrointestinal toxicity after cisplatin treatment. (A) Views of stomachs of the 3 groups. The dotted line borders the gastric fundus. (B) Gastric contents. (C) Quantity of gastric contents. (D) Gastric emptying index (GEI). (E) Feeding efficiency. Data are presented as mean ± SD, n = 8. Differences were analyzed by 1-way analysis of variance. The asterisk (*) indicates significant differences when compared with the saline group, and the hashtag (#) with cisplatin group ( P

Techniques Used:

Effects of d -methionine on hepatic lipid gene expression, muscle protein degradation, and protein synthesis–related mRNA expressions after cisplatin treatment. (A) Lipid metabolism gene expressions in liver. (B) Protein degradation– and (C) protein synthesis–related gene expressions in gastrocnemius muscle.
Figure Legend Snippet: Effects of d -methionine on hepatic lipid gene expression, muscle protein degradation, and protein synthesis–related mRNA expressions after cisplatin treatment. (A) Lipid metabolism gene expressions in liver. (B) Protein degradation– and (C) protein synthesis–related gene expressions in gastrocnemius muscle.

Techniques Used: Expressing

d -Methionine alleviated cisplatin-induced muscle mass loss and muscle atrophy. (A) Images of hind limbs. Arrowheads indicate gastrocnemius muscle. (B) Hematoxylin and eosin–stained cross sections of gastrocnemius muscle are shown at 200× magnification (bar scale = 150 µm) for calculation of fiber diameters. (C) Typical length of myofiber diameter (minor axis), the areas of 100 myotubes were measured in at least 10 fields. (D) Cross-sectional areas of at least 50 muscle fibers/animal were measured, with 6 animals analyzed for each determination. Values are presented as mean ± SD. *Indicates statistical significance when compared with the saline-treated group ( P
Figure Legend Snippet: d -Methionine alleviated cisplatin-induced muscle mass loss and muscle atrophy. (A) Images of hind limbs. Arrowheads indicate gastrocnemius muscle. (B) Hematoxylin and eosin–stained cross sections of gastrocnemius muscle are shown at 200× magnification (bar scale = 150 µm) for calculation of fiber diameters. (C) Typical length of myofiber diameter (minor axis), the areas of 100 myotubes were measured in at least 10 fields. (D) Cross-sectional areas of at least 50 muscle fibers/animal were measured, with 6 animals analyzed for each determination. Values are presented as mean ± SD. *Indicates statistical significance when compared with the saline-treated group ( P

Techniques Used: Staining

6) Product Images from "Nephroprotective Effects of Benzyl Isothiocyanate and Resveratrol Against Cisplatin-Induced Oxidative Stress and Inflammation"

Article Title: Nephroprotective Effects of Benzyl Isothiocyanate and Resveratrol Against Cisplatin-Induced Oxidative Stress and Inflammation

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2018.01268

The effects of RES and BITC treatment on serum concentrations of (A) urea and (B) creatinine in cisplatin-intoxicated mice. Data are means ± standard deviations. CDDP, cisplatin. ∗ Significantly different from the normal control group at p
Figure Legend Snippet: The effects of RES and BITC treatment on serum concentrations of (A) urea and (B) creatinine in cisplatin-intoxicated mice. Data are means ± standard deviations. CDDP, cisplatin. ∗ Significantly different from the normal control group at p

Techniques Used: Mouse Assay

H E sections of the kidney (Bar = 50 μm). (A) Saline-treated mice revealing normal kidney tissue morphology. (B) Cisplatin-treated mice revealing marked dilation and twisting of several renal tubules (arrows). (C) Slight improvement of renal tissue in CDDP–RES-treated mice (arrows). (D) Moderate histopathologic changes are seen in CDDP–BITC-treated mice (arrow). (E) Mice treated with BITC and RES combination showing mild morphologic changes. (F) Semiquantitative analysis of the histopathological changes ( ∗ significantly different from the normal control group at p
Figure Legend Snippet: H E sections of the kidney (Bar = 50 μm). (A) Saline-treated mice revealing normal kidney tissue morphology. (B) Cisplatin-treated mice revealing marked dilation and twisting of several renal tubules (arrows). (C) Slight improvement of renal tissue in CDDP–RES-treated mice (arrows). (D) Moderate histopathologic changes are seen in CDDP–BITC-treated mice (arrow). (E) Mice treated with BITC and RES combination showing mild morphologic changes. (F) Semiquantitative analysis of the histopathological changes ( ∗ significantly different from the normal control group at p

Techniques Used: Mouse Assay

The effects of RES and BITC treatment on serum and renal tissue levels of (A,B) tumor necrosis factor-α (C,D) interleukin-1β in cisplatin-intoxicated mice. Data are means ± standard deviations. CDDP, cisplatin. ∗ Significantly different from the normal control group at p
Figure Legend Snippet: The effects of RES and BITC treatment on serum and renal tissue levels of (A,B) tumor necrosis factor-α (C,D) interleukin-1β in cisplatin-intoxicated mice. Data are means ± standard deviations. CDDP, cisplatin. ∗ Significantly different from the normal control group at p

Techniques Used: Mouse Assay

COX-II immunohistochemical examination (Bar = 50 μm) of renal tissue samples from (A) saline-treated mice showing minimal COX-II expression, (B) cisplatin-intoxicated mice revealing many Cox-II-positive epithelial cells (arrows), (C) cisplatin-intoxicated mice treated with RES and (D) cisplatin-intoxicated mice treated with BITC showing moderate reductions in COX-II-positive cells (arrow), and (E) cisplatin-intoxicated mice treated with a combination of RES and BITC showing minimal COX-II expression. (F) Quantitative Cox-II expression in the cytoplasm of renal epithelial cells ( ∗ significantly different from the normal control group at p
Figure Legend Snippet: COX-II immunohistochemical examination (Bar = 50 μm) of renal tissue samples from (A) saline-treated mice showing minimal COX-II expression, (B) cisplatin-intoxicated mice revealing many Cox-II-positive epithelial cells (arrows), (C) cisplatin-intoxicated mice treated with RES and (D) cisplatin-intoxicated mice treated with BITC showing moderate reductions in COX-II-positive cells (arrow), and (E) cisplatin-intoxicated mice treated with a combination of RES and BITC showing minimal COX-II expression. (F) Quantitative Cox-II expression in the cytoplasm of renal epithelial cells ( ∗ significantly different from the normal control group at p

Techniques Used: Immunohistochemistry, Mouse Assay, Expressing

The chemical structure of (A) cisplatin, (B) resveratrol, and (C) benzyl isothiocyanate.
Figure Legend Snippet: The chemical structure of (A) cisplatin, (B) resveratrol, and (C) benzyl isothiocyanate.

Techniques Used:

7) Product Images from "Targeting the DNA Repair Endonuclease ERCC1-XPF with Green Tea Polyphenol Epigallocatechin-3-Gallate (EGCG) and Its Prodrug to Enhance Cisplatin Efficacy in Human Cancer Cells"

Article Title: Targeting the DNA Repair Endonuclease ERCC1-XPF with Green Tea Polyphenol Epigallocatechin-3-Gallate (EGCG) and Its Prodrug to Enhance Cisplatin Efficacy in Human Cancer Cells

Journal: Nutrients

doi: 10.3390/nu10111644

( A ) Structure (Left) and activity (Right) of Pro-EGCG, the EGCG prodrug containing acetylated hydroxyl groups which are cleaved by esterases upon entry into the cell, in the DNA-incision assay. Data represented as average ± standard deviation. ( B ) Titration of EGCG and Pro-EGCG in H460 cells showing the both reduce clonogenicity to approximately the same extent. ( C ). Inhibition of clonogenicity by Pro-EGCG as a single agent appears to be independent of its targeting of ERCC1/XPF as shown by titration in H1299 wild-type and ERCC1 knockout cells. ( D ) H460 cells treated with increasing concentrations of EGCG (Left) or Pro-EGCG (Right) ± a single IC 50 dose of cisplatin. All clonogenic assay data represented as average of experimental repeats ± standard deviation. Dose-response curves were compared by two-sided unpaired t -test followed by Holm’s post-hoc analysis.
Figure Legend Snippet: ( A ) Structure (Left) and activity (Right) of Pro-EGCG, the EGCG prodrug containing acetylated hydroxyl groups which are cleaved by esterases upon entry into the cell, in the DNA-incision assay. Data represented as average ± standard deviation. ( B ) Titration of EGCG and Pro-EGCG in H460 cells showing the both reduce clonogenicity to approximately the same extent. ( C ). Inhibition of clonogenicity by Pro-EGCG as a single agent appears to be independent of its targeting of ERCC1/XPF as shown by titration in H1299 wild-type and ERCC1 knockout cells. ( D ) H460 cells treated with increasing concentrations of EGCG (Left) or Pro-EGCG (Right) ± a single IC 50 dose of cisplatin. All clonogenic assay data represented as average of experimental repeats ± standard deviation. Dose-response curves were compared by two-sided unpaired t -test followed by Holm’s post-hoc analysis.

Techniques Used: Activity Assay, Standard Deviation, Titration, Inhibition, Knock-Out, Clonogenic Assay

( A ) Results from the rapid dilution assay showing GCG is a reversible inhibitor of ERCC1/XPF and EGCG is either partially reversible with slow kinetics or is irreversible. Data represented as average ± standard deviation. ( B ) Representative images of modified alkaline comet assay results for cisplatin and cisplatin + GCG in H460 cells. ( C ) Quantified data from the modified alkaline comet assay resulted in H460 cells showing inhibition of interstrand crosslink repair in cells treated with cisplatin + EGCG or cisplatin + GCG. GCG: (-)-gallocatechin gallate.
Figure Legend Snippet: ( A ) Results from the rapid dilution assay showing GCG is a reversible inhibitor of ERCC1/XPF and EGCG is either partially reversible with slow kinetics or is irreversible. Data represented as average ± standard deviation. ( B ) Representative images of modified alkaline comet assay results for cisplatin and cisplatin + GCG in H460 cells. ( C ) Quantified data from the modified alkaline comet assay resulted in H460 cells showing inhibition of interstrand crosslink repair in cells treated with cisplatin + EGCG or cisplatin + GCG. GCG: (-)-gallocatechin gallate.

Techniques Used: Dilution Assay, Standard Deviation, Modification, Alkaline Single Cell Gel Electrophoresis, Inhibition

( A ) Plot representing tumor growth of untreated, cisplatin-treated, Pro-EGCG-treated, or combination-treated mice. Data represented as tumor size (mm 3 ) over time. ( B ) Images of tumors harvested from sacrificed mice at day 19 and day 24. Growth curves were compared using a linear-mixed effects model with mice-specific effect as a random variable. P values were adjusted using Bonferroni correction. *** p
Figure Legend Snippet: ( A ) Plot representing tumor growth of untreated, cisplatin-treated, Pro-EGCG-treated, or combination-treated mice. Data represented as tumor size (mm 3 ) over time. ( B ) Images of tumors harvested from sacrificed mice at day 19 and day 24. Growth curves were compared using a linear-mixed effects model with mice-specific effect as a random variable. P values were adjusted using Bonferroni correction. *** p

Techniques Used: Mouse Assay

Raw images, ImageJ-processed images ( Top ), and quantification of immunohistochemical analysis of Ki67, TUNEL, and PCNA staining in tumors harvested from sacrificed mice ( Bottom ). Data showing increased TUNEL staining, decreased Ki67 staining, and decreased PCNA staining in the cisplatin+Pro-EGCG-treated tumors compared to other groups.
Figure Legend Snippet: Raw images, ImageJ-processed images ( Top ), and quantification of immunohistochemical analysis of Ki67, TUNEL, and PCNA staining in tumors harvested from sacrificed mice ( Bottom ). Data showing increased TUNEL staining, decreased Ki67 staining, and decreased PCNA staining in the cisplatin+Pro-EGCG-treated tumors compared to other groups.

Techniques Used: Immunohistochemistry, TUNEL Assay, Staining, Mouse Assay

8) Product Images from "Gap Junction Intercellular Communication Positively Regulates Cisplatin Toxicity by Inducing DNA Damage through Bystander Signaling"

Article Title: Gap Junction Intercellular Communication Positively Regulates Cisplatin Toxicity by Inducing DNA Damage through Bystander Signaling

Journal: Cancers

doi: 10.3390/cancers10100368

Clonogenic survival in ERCC1/XPF knockdown cells on cisplatin treatment at low and high density of cells. ( A ) A2780 and ( B ) H1299. Non-targeting siRNA (siC) and ERCC1-XPF siRNA transfected cells (siX + siE) transfected cells were treated to cisplatin at high density and low density and plated for colony survival as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments.
Figure Legend Snippet: Clonogenic survival in ERCC1/XPF knockdown cells on cisplatin treatment at low and high density of cells. ( A ) A2780 and ( B ) H1299. Non-targeting siRNA (siC) and ERCC1-XPF siRNA transfected cells (siX + siE) transfected cells were treated to cisplatin at high density and low density and plated for colony survival as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments.

Techniques Used: Transfection

Positive γ-H2AX foci indicating DNA DSB formation in bystander cells post-cisplatin treatment. ( A ) H1355 and ( B ) A2780 cells were divided into 2 populations—labeled with vital cell tracker dye or left unstained. Labeled cells were either treated or left untreated (control) to cisplatin (CDDP) and then mixed with unstained untreated cells and then visualized for positive γ-H2AX foci by immunostaining. Values are represented as percent above background ± S.D. from 3 independent experiments. ( C ) Representative image from H1355 cells. Left panel is without cisplatin/vehicle while right panel is cisplatin treated. Blue—DAPI, red/orange—cell tracker orange, green—γ-H2AX foci merged. ( D , E ) DSB formation in H1355, Cx43 knockdown cells ( D ) and cells plated at colony density ( E ). In both cases, cell were divided into 2 populations—labeled with vital cell tracker dye or left unstained. Labeled cells were either treated or left untreated (control) to cisplatin and then mixed with unstained untreated cells and then visualized for positive γ-H2AX foci by immunostaining. Values are represented as percent above background ± S.D. from 3 independent experiments.
Figure Legend Snippet: Positive γ-H2AX foci indicating DNA DSB formation in bystander cells post-cisplatin treatment. ( A ) H1355 and ( B ) A2780 cells were divided into 2 populations—labeled with vital cell tracker dye or left unstained. Labeled cells were either treated or left untreated (control) to cisplatin (CDDP) and then mixed with unstained untreated cells and then visualized for positive γ-H2AX foci by immunostaining. Values are represented as percent above background ± S.D. from 3 independent experiments. ( C ) Representative image from H1355 cells. Left panel is without cisplatin/vehicle while right panel is cisplatin treated. Blue—DAPI, red/orange—cell tracker orange, green—γ-H2AX foci merged. ( D , E ) DSB formation in H1355, Cx43 knockdown cells ( D ) and cells plated at colony density ( E ). In both cases, cell were divided into 2 populations—labeled with vital cell tracker dye or left unstained. Labeled cells were either treated or left untreated (control) to cisplatin and then mixed with unstained untreated cells and then visualized for positive γ-H2AX foci by immunostaining. Values are represented as percent above background ± S.D. from 3 independent experiments.

Techniques Used: Labeling, Immunostaining

Clonogenic survival at high- and low-density post Cx43 knockdown. ( A ) H1355, ( B ) H460, ( C ) A2780 cells. Non-targeting siRNA transfected (siC) and siCx43 transfected cells were treated to cisplatin at high density and low density and plated for colony survival as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments, each plated in triplicate.
Figure Legend Snippet: Clonogenic survival at high- and low-density post Cx43 knockdown. ( A ) H1355, ( B ) H460, ( C ) A2780 cells. Non-targeting siRNA transfected (siC) and siCx43 transfected cells were treated to cisplatin at high density and low density and plated for colony survival as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments, each plated in triplicate.

Techniques Used: Transfection

Clonogenic survival after cisplatin treatment at low and high density of cells. ( A ) H1355, ( B ) H460, ( C ) H1299, ( D ) A2780. Clonogenic survival was performed at high-density and low-density cisplatin treatment as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments.
Figure Legend Snippet: Clonogenic survival after cisplatin treatment at low and high density of cells. ( A ) H1355, ( B ) H460, ( C ) H1299, ( D ) A2780. Clonogenic survival was performed at high-density and low-density cisplatin treatment as described in the methods section. Calculated IC 50 values are represented in each figure for each cell line. Values are represented as mean ± SEM from three independent experiments.

Techniques Used:

9) Product Images from "Liposomes Loaded with Cisplatin and Magnetic Nanoparticles: Physicochemical Characterization, Pharmacokinetics, and In-Vitro Efficacy"

Article Title: Liposomes Loaded with Cisplatin and Magnetic Nanoparticles: Physicochemical Characterization, Pharmacokinetics, and In-Vitro Efficacy

Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

doi: 10.3390/molecules23092272

Differential scanning calorimetry of liposome suspensions. Empty liposomes (Ls: —), cisplatin-loaded liposomes (Cis-Ls: ···), blank magnetoliposomes (-- · --), and cisplatin-loaded magnetic liposomes (Cis-MLs: ---).
Figure Legend Snippet: Differential scanning calorimetry of liposome suspensions. Empty liposomes (Ls: —), cisplatin-loaded liposomes (Cis-Ls: ···), blank magnetoliposomes (-- · --), and cisplatin-loaded magnetic liposomes (Cis-MLs: ---).

Techniques Used:

In vitro drug release profiles of cisplatin-loaded liposomes (Cis-Ls, white dots) and cisplatin-loaded magnetic liposomes (Cis-MLs, black dots). ( a ) Percentage of cisplatin released after 48 h of incubation at room temperature in saline solution; ( b ) Percentage of cisplatin released after 48 h of incubation at 37 °C in human serum. Values are expressed as the mean ± SEM ( n = 3).
Figure Legend Snippet: In vitro drug release profiles of cisplatin-loaded liposomes (Cis-Ls, white dots) and cisplatin-loaded magnetic liposomes (Cis-MLs, black dots). ( a ) Percentage of cisplatin released after 48 h of incubation at room temperature in saline solution; ( b ) Percentage of cisplatin released after 48 h of incubation at 37 °C in human serum. Values are expressed as the mean ± SEM ( n = 3).

Techniques Used: In Vitro, Incubation

Cisplatin plasma concentrations versus time curves in rats subsequent to intravenous (i.v.) administration of cisplatin solution, cisplatin-loaded liposomes (Cis-Ls), or cisplatin magnetic liposomes (Cis-MLs). Iron plasma concentration versus time curve after i.v. administration of Cis-MLs. The dose injected corresponds to 6 mg/kg cisplatin and 2 mg/kg iron. Values are expressed as the mean ± SEM ( n = 5–6).
Figure Legend Snippet: Cisplatin plasma concentrations versus time curves in rats subsequent to intravenous (i.v.) administration of cisplatin solution, cisplatin-loaded liposomes (Cis-Ls), or cisplatin magnetic liposomes (Cis-MLs). Iron plasma concentration versus time curve after i.v. administration of Cis-MLs. The dose injected corresponds to 6 mg/kg cisplatin and 2 mg/kg iron. Values are expressed as the mean ± SEM ( n = 5–6).

Techniques Used: Concentration Assay, Injection

Representative TEM micrographs of ( a ) cisplatin-loaded liposomes (Cis-Ls) and ( b , c ) cisplatin-loaded magnetic liposomes (Cis-MLs). All samples were negatively stained with 2% uranyl acetate solution. The inset represents an enlarged view of the magnetite nanoparticles contained in the liposome structure.
Figure Legend Snippet: Representative TEM micrographs of ( a ) cisplatin-loaded liposomes (Cis-Ls) and ( b , c ) cisplatin-loaded magnetic liposomes (Cis-MLs). All samples were negatively stained with 2% uranyl acetate solution. The inset represents an enlarged view of the magnetite nanoparticles contained in the liposome structure.

Techniques Used: Transmission Electron Microscopy, Staining

( a ) Cisplatin accumulation in tissues 96 h after administration of cisplatin-loaded liposomes (Cis-Ls, white bars) or cisplatin-loaded magnetic liposomes (Cis-MLs, black bars); in both cases, the injected dose corresponds to 6 mg/kg cisplatin and 2 mg/kg iron; ( b ) Remaining weight versus time following the administration of Cis-Ls (white dots), Cis-MLs (black dots), and control group (animals without any treatment, open triangles). The animals were weighed before the liposome injection and every 24 h post-administration. Values are expressed as the mean ± SEM ( n = 5–6).
Figure Legend Snippet: ( a ) Cisplatin accumulation in tissues 96 h after administration of cisplatin-loaded liposomes (Cis-Ls, white bars) or cisplatin-loaded magnetic liposomes (Cis-MLs, black bars); in both cases, the injected dose corresponds to 6 mg/kg cisplatin and 2 mg/kg iron; ( b ) Remaining weight versus time following the administration of Cis-Ls (white dots), Cis-MLs (black dots), and control group (animals without any treatment, open triangles). The animals were weighed before the liposome injection and every 24 h post-administration. Values are expressed as the mean ± SEM ( n = 5–6).

Techniques Used: Injection

( a ) Cell viability at 72 h post-treatment with liposomes only (Ls, control), cisplatin-loaded liposomes (Cis-Ls), cisplatin-loaded magnetic liposomes (Cis-MLs), and Cis-MLs plus magnetic hyperthermia treatment with an alternating current magnetic field (AMF) (Cis-MLs + AFM); ( b ) Percentage of apoptotic cells at 72 h after treatment with liposomes only (Ls, control), cisplatin-loaded liposomes (Cis-Ls), cisplatin-loaded magnetic liposomes (Cis-MLs), and Cis-MLs plus magnetic hyperthermia treatment (Cis-MLS + AFM). Values are expressed as the mean ± SEM of three individual experiments. ( * ) Indicates a significant difference ( p
Figure Legend Snippet: ( a ) Cell viability at 72 h post-treatment with liposomes only (Ls, control), cisplatin-loaded liposomes (Cis-Ls), cisplatin-loaded magnetic liposomes (Cis-MLs), and Cis-MLs plus magnetic hyperthermia treatment with an alternating current magnetic field (AMF) (Cis-MLs + AFM); ( b ) Percentage of apoptotic cells at 72 h after treatment with liposomes only (Ls, control), cisplatin-loaded liposomes (Cis-Ls), cisplatin-loaded magnetic liposomes (Cis-MLs), and Cis-MLs plus magnetic hyperthermia treatment (Cis-MLS + AFM). Values are expressed as the mean ± SEM of three individual experiments. ( * ) Indicates a significant difference ( p

Techniques Used:

10) Product Images from "Lycium europaeum Extract: A New Potential Antioxidant Source against Cisplatin-Induced Liver and Kidney Injuries in Mice"

Article Title: Lycium europaeum Extract: A New Potential Antioxidant Source against Cisplatin-Induced Liver and Kidney Injuries in Mice

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2018/1630751

Effects of the methanol extract of leaves from Lycium europaeum (LEM) on kidney histology in cisplatin-intoxicated mice. Kidneys were sectioned and stained with hematoxylin-eosin (H E). Representative photographs (200x) from the control group (a), 150 mg/kg BW LEM group (b); cisplatin-treated group (c), 150 mg/kg BW LEM + cisplatin group (d), and 50 mg/kg BW quercetin-positive control group (e). GA: glomerular atrophy; DL: tubular dilation; G: glomerule; D: distal convoluted tubules; P: proximal convoluted tubules; C: coast.
Figure Legend Snippet: Effects of the methanol extract of leaves from Lycium europaeum (LEM) on kidney histology in cisplatin-intoxicated mice. Kidneys were sectioned and stained with hematoxylin-eosin (H E). Representative photographs (200x) from the control group (a), 150 mg/kg BW LEM group (b); cisplatin-treated group (c), 150 mg/kg BW LEM + cisplatin group (d), and 50 mg/kg BW quercetin-positive control group (e). GA: glomerular atrophy; DL: tubular dilation; G: glomerule; D: distal convoluted tubules; P: proximal convoluted tubules; C: coast.

Techniques Used: Mouse Assay, Staining, Positive Control

Lipid peroxidation and antioxidant enzyme activities in liver and kidney tissues of mice treated with cisplatin. Values were expressed as the mean ± SD ( n = 6). ++ Significant difference at p
Figure Legend Snippet: Lipid peroxidation and antioxidant enzyme activities in liver and kidney tissues of mice treated with cisplatin. Values were expressed as the mean ± SD ( n = 6). ++ Significant difference at p

Techniques Used: Mouse Assay

Effects of the methanol extract of leaves from Lycium europaeum (LEM) on the hepatic histology in CCl 4 -intoxicated mice. Livers were sectioned and stained with hematoxylin-eosin (H E). Representative photographs (200x) from the control group (a), 150 mg/kg BW LEM group (b), cisplatin-treated group (c), 150 mg/kg BW LEM + cisplatin group (d), and 50 mg/kg BW quercetin-positive control group (e). MD: membrane cell degradation; IL: inflammatory leukocyte infiltrations; CV: central vein.
Figure Legend Snippet: Effects of the methanol extract of leaves from Lycium europaeum (LEM) on the hepatic histology in CCl 4 -intoxicated mice. Livers were sectioned and stained with hematoxylin-eosin (H E). Representative photographs (200x) from the control group (a), 150 mg/kg BW LEM group (b), cisplatin-treated group (c), 150 mg/kg BW LEM + cisplatin group (d), and 50 mg/kg BW quercetin-positive control group (e). MD: membrane cell degradation; IL: inflammatory leukocyte infiltrations; CV: central vein.

Techniques Used: Mouse Assay, Staining, Positive Control

11) Product Images from "Cisplatin-induced oxidative stress stimulates renal Fas ligand shedding"

Article Title: Cisplatin-induced oxidative stress stimulates renal Fas ligand shedding

Journal: Renal Failure

doi: 10.1080/0886022X.2018.1456938

Cisplatin induces ROS-dependent kidney injury in mice. Bar graphs showing (A) kidney-to-body weight ratio, and the levels of plasma creatinine (B) and BUN (C), urinary NGAL (D), cystatin C (E), and albumin-creatinine-ratio (ACR; F) in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p
Figure Legend Snippet: Cisplatin induces ROS-dependent kidney injury in mice. Bar graphs showing (A) kidney-to-body weight ratio, and the levels of plasma creatinine (B) and BUN (C), urinary NGAL (D), cystatin C (E), and albumin-creatinine-ratio (ACR; F) in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p

Techniques Used: Mouse Assay, Injection

Cisplatin promotes oxidative DNA damage and renal lipid peroxidation in mice. Bar graphs summarizing: A, Urinary 8-OHdG and B, kidney MDA concentrations in Captisol (vehicle control)-, cisplatin-, and TEMPOL + cisplatin-treated mice. Mice were pretreated with TEMPOL (100 mg/kg; IP) 1 h before a single IP injection of cisplatin (15 mg/kg). Thereafter, the animals received a daily injection of TEMPOL for 4 days. * p
Figure Legend Snippet: Cisplatin promotes oxidative DNA damage and renal lipid peroxidation in mice. Bar graphs summarizing: A, Urinary 8-OHdG and B, kidney MDA concentrations in Captisol (vehicle control)-, cisplatin-, and TEMPOL + cisplatin-treated mice. Mice were pretreated with TEMPOL (100 mg/kg; IP) 1 h before a single IP injection of cisplatin (15 mg/kg). Thereafter, the animals received a daily injection of TEMPOL for 4 days. * p

Techniques Used: Mouse Assay, Multiple Displacement Amplification, Injection

Cisplatin-induced oxidative stress increases urinary sFasL in mice. Bar graphs summarizing the levels of sFasL in: (A) Plasma, and (B) Urine of Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p
Figure Legend Snippet: Cisplatin-induced oxidative stress increases urinary sFasL in mice. Bar graphs summarizing the levels of sFasL in: (A) Plasma, and (B) Urine of Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p

Techniques Used: Mouse Assay, Injection

Cisplatin elicits ROS-dependent tubular damage and renal apoptosis in mice. (A) Images (PAS staining) and (B) average tubular injury score in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. Cisplatin-treated groups showed variable tubular injury in the form of vacuolar degeneration and necrosis (arrows). However, TEMPOL ameliorated the severity of cisplatin-induced injury where few necrotic lesions were observed (arrow). (C) Representative confocal microscopy images, and (D) Bar graphs showing TUNEL staining and mean TUNEL positive cells/sq µm in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p
Figure Legend Snippet: Cisplatin elicits ROS-dependent tubular damage and renal apoptosis in mice. (A) Images (PAS staining) and (B) average tubular injury score in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. Cisplatin-treated groups showed variable tubular injury in the form of vacuolar degeneration and necrosis (arrows). However, TEMPOL ameliorated the severity of cisplatin-induced injury where few necrotic lesions were observed (arrow). (C) Representative confocal microscopy images, and (D) Bar graphs showing TUNEL staining and mean TUNEL positive cells/sq µm in Captisol (vehicle control)-, cisplatin (15 mg/kg; single IP injection)-, and TEMPOL (100 mg/kg; IP for 4 days) + cisplatin-treated mice. * p

Techniques Used: Mouse Assay, Staining, Injection, Confocal Microscopy, TUNEL Assay

ROS scavenger mitigates cisplatin-induced human proximal tubule cell death. (A) Live content cell images (phase contrast and green fluorescent staining of nuclear DNA in apoptotic cells), and (B) kinetic curves ( n = 5 each) demonstrating that cisplatin (30 µM) induces time-dependent increase in caspase-3/7 activity in HK-2 cells; effects abrogated by TEMPOL (1 mM), Fas blocking antibody (Fas BA; 10 µg/mL), caspase (Casp) inhibitor (Ac-DEVD-CHO; 50 µM), and AG 14361 (PARP1 inhibitor; 300 nM). (C) bar graphs ( n = 5 each) summarizing percent cytotoxicity (LDH release) in Captisol (vehicle control)-, cisplatin (30 µM)-, and TEMPOL (1 mM) + cisplatin-, Fas BA (10 µg/mL) + cisplatin-, Casp inhibitor (50 µM) + cisplatin-, and AG 14361 (300 nM) + cisplatin-treated HK-2 cells. * p
Figure Legend Snippet: ROS scavenger mitigates cisplatin-induced human proximal tubule cell death. (A) Live content cell images (phase contrast and green fluorescent staining of nuclear DNA in apoptotic cells), and (B) kinetic curves ( n = 5 each) demonstrating that cisplatin (30 µM) induces time-dependent increase in caspase-3/7 activity in HK-2 cells; effects abrogated by TEMPOL (1 mM), Fas blocking antibody (Fas BA; 10 µg/mL), caspase (Casp) inhibitor (Ac-DEVD-CHO; 50 µM), and AG 14361 (PARP1 inhibitor; 300 nM). (C) bar graphs ( n = 5 each) summarizing percent cytotoxicity (LDH release) in Captisol (vehicle control)-, cisplatin (30 µM)-, and TEMPOL (1 mM) + cisplatin-, Fas BA (10 µg/mL) + cisplatin-, Casp inhibitor (50 µM) + cisplatin-, and AG 14361 (300 nM) + cisplatin-treated HK-2 cells. * p

Techniques Used: Staining, Activity Assay, Blocking Assay

12) Product Images from "Protective Effect of D-Methionine on Body Weight Loss, Anorexia, and Nephrotoxicity in Cisplatin-Induced Chronic Toxicity in Rats"

Article Title: Protective Effect of D-Methionine on Body Weight Loss, Anorexia, and Nephrotoxicity in Cisplatin-Induced Chronic Toxicity in Rats

Journal: Integrative Cancer Therapies

doi: 10.1177/1534735417753543

Effect of D-methionine on body weight (A), food intake (B), and feeding efficiency (C) after cisplatin injection. All animals were sacrificed on the 21sh day of the experiment and body weight and food intake were recorded. *Indicates statistical significance when compared with the control group ( P
Figure Legend Snippet: Effect of D-methionine on body weight (A), food intake (B), and feeding efficiency (C) after cisplatin injection. All animals were sacrificed on the 21sh day of the experiment and body weight and food intake were recorded. *Indicates statistical significance when compared with the control group ( P

Techniques Used: Injection

Effects of D-methionine on catalase activity (A), GSH concentration (B), lipid peroxidation (C) in the kidney, and serum triglyceride concentration (D) in cisplatin-induced nephrotoxicity. Values are presented as mean ± SD. *Indicates statistical significance when compared with the control group ( P
Figure Legend Snippet: Effects of D-methionine on catalase activity (A), GSH concentration (B), lipid peroxidation (C) in the kidney, and serum triglyceride concentration (D) in cisplatin-induced nephrotoxicity. Values are presented as mean ± SD. *Indicates statistical significance when compared with the control group ( P

Techniques Used: Activity Assay, Concentration Assay

13) Product Images from "Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells"

Article Title: Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0182809

BIK is involved in DNA damage-induced apoptosis in HCT-116 wt cells, but not in HCT-116 p53 -/- cells. (A) HCT-116 wt and HCT-116 p53 -/- cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 0-12h and BIK protein levels were detected by immunoblot analysis. Actin was probed as a loading control. (B) HCT-116 wt and HCT-116 p53 -/- cells were transiently transfected with BIK siRNA or scrambled siRNA for 48h. The efficiency of knockdown was monitored by immunoblots. (C) BIK siRNA-transfected or scrambled siRNA-transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 48h and cell viability was evaluated by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, **P
Figure Legend Snippet: BIK is involved in DNA damage-induced apoptosis in HCT-116 wt cells, but not in HCT-116 p53 -/- cells. (A) HCT-116 wt and HCT-116 p53 -/- cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 0-12h and BIK protein levels were detected by immunoblot analysis. Actin was probed as a loading control. (B) HCT-116 wt and HCT-116 p53 -/- cells were transiently transfected with BIK siRNA or scrambled siRNA for 48h. The efficiency of knockdown was monitored by immunoblots. (C) BIK siRNA-transfected or scrambled siRNA-transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 48h and cell viability was evaluated by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, **P

Techniques Used: Transfection, Western Blot

BIK mediates cisplatin-induced cell death in HCT-116 wt cellular spheroids, but not in HCT-116 p53 -/- spheroids. (A) HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. Cells were subsequently grown in 24-well 3D Algimatrix plates in the presence of RNAi duplexes. Microscopic evaluation of spheroids was done to verify that siRNA treatments did not interfere with the 3D growth of HCT-116 cells. (B) The efficiency of BIK depletion by RNA interference in HCT-116 wt and HCT-116 p53 -/- was determined by immunoblot analysis. Actin was probed as loading control. (C) Spheroids were treated with cisplatin (200 μM) for 48h and cell viability was assessed by using alamarBlue assay (mean±SEM, n = 3, *P
Figure Legend Snippet: BIK mediates cisplatin-induced cell death in HCT-116 wt cellular spheroids, but not in HCT-116 p53 -/- spheroids. (A) HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. Cells were subsequently grown in 24-well 3D Algimatrix plates in the presence of RNAi duplexes. Microscopic evaluation of spheroids was done to verify that siRNA treatments did not interfere with the 3D growth of HCT-116 cells. (B) The efficiency of BIK depletion by RNA interference in HCT-116 wt and HCT-116 p53 -/- was determined by immunoblot analysis. Actin was probed as loading control. (C) Spheroids were treated with cisplatin (200 μM) for 48h and cell viability was assessed by using alamarBlue assay (mean±SEM, n = 3, *P

Techniques Used: Transfection, Alamar Blue Assay

Cisplatin induces early LMP in HCT-116 p53 -/- cells. (A) HCT-116 wt and HCT-116 p53-/- cells were treated with cisplatin (20 μM) for 1h. HCT-116 p53 -/- cells were TIRON (10 mM) for 2h and then treated with cisplatin for 1h to examine the effect of TIRON on cisplatin-induced LMP. Cells were stained for galectin-3 to evaluate the lysosomal membrane permeabilization. (B) HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. Cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 1h and the Cathepsin B/L activity was measured in untransfected and transfected cells (mean RFU±SEM, n = 3). (C) HCT-116 p53 -/- cells were pretreated with CA-074Me (100 μM) or Z-FA-FMK (10 μM) for 2h and then treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 48h. Cell viability was determined by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, *P
Figure Legend Snippet: Cisplatin induces early LMP in HCT-116 p53 -/- cells. (A) HCT-116 wt and HCT-116 p53-/- cells were treated with cisplatin (20 μM) for 1h. HCT-116 p53 -/- cells were TIRON (10 mM) for 2h and then treated with cisplatin for 1h to examine the effect of TIRON on cisplatin-induced LMP. Cells were stained for galectin-3 to evaluate the lysosomal membrane permeabilization. (B) HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. Cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 1h and the Cathepsin B/L activity was measured in untransfected and transfected cells (mean RFU±SEM, n = 3). (C) HCT-116 p53 -/- cells were pretreated with CA-074Me (100 μM) or Z-FA-FMK (10 μM) for 2h and then treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 48h. Cell viability was determined by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, *P

Techniques Used: Staining, Transfection, Activity Assay

DNA damage induces biphasic ROS production in HCT-116 wt cells. HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. (A) Untransfected and transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) and total ROS formation was monitored by using DCF-DA probe. Kinetic tracing was processed by measurements in every 15 min for 12h (mean RFU±SEM, n = 3) (B) Untransfected and transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) and superoxide formation was monitored by MitoSOX Red probe. Kinetic tracing was processed by measurements in every 15 min for 12h (mean RFU±SEM, n = 3). (C) Cells were pretreated with NAC (10 mM) or TIRON (10 mM) for 2h and then treated with cisplatin for 48h. Cell viability was evaluated by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, *P
Figure Legend Snippet: DNA damage induces biphasic ROS production in HCT-116 wt cells. HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. (A) Untransfected and transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) and total ROS formation was monitored by using DCF-DA probe. Kinetic tracing was processed by measurements in every 15 min for 12h (mean RFU±SEM, n = 3) (B) Untransfected and transfected cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) and superoxide formation was monitored by MitoSOX Red probe. Kinetic tracing was processed by measurements in every 15 min for 12h (mean RFU±SEM, n = 3). (C) Cells were pretreated with NAC (10 mM) or TIRON (10 mM) for 2h and then treated with cisplatin for 48h. Cell viability was evaluated by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, *P

Techniques Used: Transfection

BIK/BCL-2 and BIK/BCL-XL interactions were increased in HCT-116 wt cells in response to DNA damage. HCT-116 wt and HCT-116 p53 -/- cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 4h and the interaction of BIK with BCL-2, BCL-XL, and MCL-1 was detected by coimmunoprecipitation assays. Inputs for coimmunoprecipitation experiments were also subjected to immunoblot analysis and actin was probed as loading control.
Figure Legend Snippet: BIK/BCL-2 and BIK/BCL-XL interactions were increased in HCT-116 wt cells in response to DNA damage. HCT-116 wt and HCT-116 p53 -/- cells were treated with cisplatin (20 μM) or UV (100 mJ/cm 2 ) for 4h and the interaction of BIK with BCL-2, BCL-XL, and MCL-1 was detected by coimmunoprecipitation assays. Inputs for coimmunoprecipitation experiments were also subjected to immunoblot analysis and actin was probed as loading control.

Techniques Used:

14) Product Images from "Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells"

Article Title: Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells

Journal: Journal of Ginseng Research

doi: 10.1016/j.jgr.2017.01.011

Western blot analysis of the levels of p-JNK, JNK, p-ERK, ERK, p-p38, p38, and cleaved caspase-3 in LLC-PK1 cells treated with ginsenoside Rh3. Results of the Western blot analysis show the levels of phosphorylated (p)-JNK, JNK, p-ERK, ERK, p-p38, p38, cleaved caspase-3, and GAPDH in LLC-PK1 cells treated with ginsenoside Rh3 with or without cisplatin at different concentrations for 24 h. Whole cell lysates (20 μg) were separated using SDS-PAGE, transferred onto PVDF transfer membranes, and probed with the indicated antibodies. Proteins were visualized using an ECL detection system. * p
Figure Legend Snippet: Western blot analysis of the levels of p-JNK, JNK, p-ERK, ERK, p-p38, p38, and cleaved caspase-3 in LLC-PK1 cells treated with ginsenoside Rh3. Results of the Western blot analysis show the levels of phosphorylated (p)-JNK, JNK, p-ERK, ERK, p-p38, p38, cleaved caspase-3, and GAPDH in LLC-PK1 cells treated with ginsenoside Rh3 with or without cisplatin at different concentrations for 24 h. Whole cell lysates (20 μg) were separated using SDS-PAGE, transferred onto PVDF transfer membranes, and probed with the indicated antibodies. Proteins were visualized using an ECL detection system. * p

Techniques Used: Western Blot, SDS Page

Comparison of the kidney-protective effects of ginsenosides Rk2 and Rh3 in LLC-PK1 cells. (A) Chemical structures of ginsenosides Rk2 and Rh3. (B) Comparison of protective effects of ginsenosides Rk2 and Rh3 against cisplatin-induced cytotoxicity in LLC-PK1 cells. LLC-PK1 cells were pretreated with various concentrations of ginsenosides Rk2 and Rh3 for 2 h, and then further treated with 25μM of cisplatin for 24 h. Cell viability was assessed using the MTT assay. NAC was used as a positive control compound. * p
Figure Legend Snippet: Comparison of the kidney-protective effects of ginsenosides Rk2 and Rh3 in LLC-PK1 cells. (A) Chemical structures of ginsenosides Rk2 and Rh3. (B) Comparison of protective effects of ginsenosides Rk2 and Rh3 against cisplatin-induced cytotoxicity in LLC-PK1 cells. LLC-PK1 cells were pretreated with various concentrations of ginsenosides Rk2 and Rh3 for 2 h, and then further treated with 25μM of cisplatin for 24 h. Cell viability was assessed using the MTT assay. NAC was used as a positive control compound. * p

Techniques Used: MTT Assay, Positive Control

15) Product Images from "Galectin-1-Induced Autophagy Facilitates Cisplatin Resistance of Hepatocellular Carcinoma"

Article Title: Galectin-1-Induced Autophagy Facilitates Cisplatin Resistance of Hepatocellular Carcinoma

Journal: PLoS ONE

doi: 10.1371/journal.pone.0148408

Autophagy contributes to galectin-1-induced cisplatin resistance of hepatoma cells. (A) Atg5 protein was knocked down in Huh-7 cells by shRNA (clone 5). Huh-7-shLuc and Huh-7-shAtg5, cells were pretreated with galectin-1 (10 μg/ml) for 1 hour, and then further treated with cisplatin for another 24 hours. The cell death was determined by PI staining. (B) HepG2 cells were pretreated with autophagy inhibitor bafilomycin A1 (25 nM) for 1 hour and then treated with galactin-1 (10 μg/ml) and cisplatin. After 24 hours post treatment, the cell death was determined by PI staining. (C) Wild-type (WT) and Atg5-/- cells were pretreated with galectin-1 (10 μg/ml) for 1 hour and then further treated with cisplatin (16 μg/ml) for another 24 hours. The cell death rate was measured by PI staining. * p
Figure Legend Snippet: Autophagy contributes to galectin-1-induced cisplatin resistance of hepatoma cells. (A) Atg5 protein was knocked down in Huh-7 cells by shRNA (clone 5). Huh-7-shLuc and Huh-7-shAtg5, cells were pretreated with galectin-1 (10 μg/ml) for 1 hour, and then further treated with cisplatin for another 24 hours. The cell death was determined by PI staining. (B) HepG2 cells were pretreated with autophagy inhibitor bafilomycin A1 (25 nM) for 1 hour and then treated with galactin-1 (10 μg/ml) and cisplatin. After 24 hours post treatment, the cell death was determined by PI staining. (C) Wild-type (WT) and Atg5-/- cells were pretreated with galectin-1 (10 μg/ml) for 1 hour and then further treated with cisplatin (16 μg/ml) for another 24 hours. The cell death rate was measured by PI staining. * p

Techniques Used: shRNA, Staining

Model of galectin-1-induced autophagy triggers cisplatin resistance. In hepatoma microenvironment, cisplatin can stimulate hepatoma cells to undergo mitochondria-mediated apoptosis. However, free form galectin-1 secreted by stroma cells or hepatoma cells can bind to hepatoma cells and trigger autophagic flux via inhibiting AKT-mTOR activities. Galectin-1-induced autophagy can target cisplatin- damaged mitochondria to reduce both mitochondrial membrane potential loss and cell death, thus providing a chemoresistance to cancer cells.
Figure Legend Snippet: Model of galectin-1-induced autophagy triggers cisplatin resistance. In hepatoma microenvironment, cisplatin can stimulate hepatoma cells to undergo mitochondria-mediated apoptosis. However, free form galectin-1 secreted by stroma cells or hepatoma cells can bind to hepatoma cells and trigger autophagic flux via inhibiting AKT-mTOR activities. Galectin-1-induced autophagy can target cisplatin- damaged mitochondria to reduce both mitochondrial membrane potential loss and cell death, thus providing a chemoresistance to cancer cells.

Techniques Used:

Galectin-1 attenuates cisplatin-induced cell death of hepatoma cells. (A) HepG2 and Huh7 cells were treated with various concentrations of cisplatin for 24 hours. The cell death rate was measured by PI (propidium iodide) staining using flow cytometry. (B) HepG2 and Huh7 cells were pretreated with galectin-1 for 1 hour followed by the treatment with cisplatin for 24 hours. The cell death was determined by PI staining. (C D) Huh 7 cells were pretreated with respective soluble galectin-1 inhibitors, including β-lactose and TDG, for 1 hour and further treated with cisplatin in the absence or presence of galectin-1 for another 24 hours. The cell death was determined through PI staining. The data shown are the mean ± SEM values of 3 experiments. * p
Figure Legend Snippet: Galectin-1 attenuates cisplatin-induced cell death of hepatoma cells. (A) HepG2 and Huh7 cells were treated with various concentrations of cisplatin for 24 hours. The cell death rate was measured by PI (propidium iodide) staining using flow cytometry. (B) HepG2 and Huh7 cells were pretreated with galectin-1 for 1 hour followed by the treatment with cisplatin for 24 hours. The cell death was determined by PI staining. (C D) Huh 7 cells were pretreated with respective soluble galectin-1 inhibitors, including β-lactose and TDG, for 1 hour and further treated with cisplatin in the absence or presence of galectin-1 for another 24 hours. The cell death was determined through PI staining. The data shown are the mean ± SEM values of 3 experiments. * p

Techniques Used: Staining, Flow Cytometry, Cytometry

Galectin-1 enhances mitophagy to reduce cisplatin-triggered apoptosis. (A) HepG2 cells were pretreated with autophagy inhibitor bafilomycin A1 (25 nM) for 1 hour, and then further treated with galectin-1 (10 μg/ml) and cisplatin for the indicated time. The depolarized mitochondrial membrane percentage was measured by JC-1 staining and quantified. (B) Huh-7 and HepG2 cells followed above experiment treatment. The cell apoptosis (sub-G1 phase %) was measured by PI staining after 70% alcohol fixation at -20°C overnight. (C) mRFP-GFP-LC3 plasmids were introduced into HepG2 cells by lentiviral vectors and treated with galectin-1 (10 μg/ml) for 1 hour and then treated with cisplatin (16 μg/ml) for another 3 hours. Cells were then fixed and stained with anti-Tom20 antibody. The protein distribution was analyzed under the confocal microscope. White arrows indicate the targeted mitochondria by autophagosome. The quantification results were calculated from 3 individual experiments.* p
Figure Legend Snippet: Galectin-1 enhances mitophagy to reduce cisplatin-triggered apoptosis. (A) HepG2 cells were pretreated with autophagy inhibitor bafilomycin A1 (25 nM) for 1 hour, and then further treated with galectin-1 (10 μg/ml) and cisplatin for the indicated time. The depolarized mitochondrial membrane percentage was measured by JC-1 staining and quantified. (B) Huh-7 and HepG2 cells followed above experiment treatment. The cell apoptosis (sub-G1 phase %) was measured by PI staining after 70% alcohol fixation at -20°C overnight. (C) mRFP-GFP-LC3 plasmids were introduced into HepG2 cells by lentiviral vectors and treated with galectin-1 (10 μg/ml) for 1 hour and then treated with cisplatin (16 μg/ml) for another 3 hours. Cells were then fixed and stained with anti-Tom20 antibody. The protein distribution was analyzed under the confocal microscope. White arrows indicate the targeted mitochondria by autophagosome. The quantification results were calculated from 3 individual experiments.* p

Techniques Used: Staining, Microscopy

Galectin-1 inhibitor increases anticancer activity of cisplatin in hepatoma-bearing mice. (A) 8–10 week old BABL/C mice were intrasplenically inoculated with mouse hepatoma cells ML-1 4a to establish tumor nodule formation (n = 8). Cisplatin (5mg/kg) was given to mice twice at a 7- day interval beginning on day 7. TDG (240mg/kg) was given to mice on day 6, 10 and 17. The number and sizes of the tumor nodules in the liver were determined on day 28. (B-C) After 28 days of treatment, mice were sacrificed and the livers were sectioned to analyze the number and size of live nodules. Results were quantified from three independent experiments.
Figure Legend Snippet: Galectin-1 inhibitor increases anticancer activity of cisplatin in hepatoma-bearing mice. (A) 8–10 week old BABL/C mice were intrasplenically inoculated with mouse hepatoma cells ML-1 4a to establish tumor nodule formation (n = 8). Cisplatin (5mg/kg) was given to mice twice at a 7- day interval beginning on day 7. TDG (240mg/kg) was given to mice on day 6, 10 and 17. The number and sizes of the tumor nodules in the liver were determined on day 28. (B-C) After 28 days of treatment, mice were sacrificed and the livers were sectioned to analyze the number and size of live nodules. Results were quantified from three independent experiments.

Techniques Used: Activity Assay, Mouse Assay

16) Product Images from "Small-molecule inhibitor of Bcl-2 (TW-37) suppresses growth and enhances cisplatin-induced apoptosis in ovarian cancer cells"

Article Title: Small-molecule inhibitor of Bcl-2 (TW-37) suppresses growth and enhances cisplatin-induced apoptosis in ovarian cancer cells

Journal: Journal of Ovarian Research

doi: 10.1186/s13048-015-0130-x

Ovarian cancer cells have differing levels of native resistance to cisplatin. Human OC cell lines SKOV3, OVCAR3, OV-90, 3AO and SKOV3 DDP were treated with increasing concentrations of cisplatin (0–500 umol/L) for 72 h. The viabilities indicated on the y axis were determined by MTT assays and normalized to control. Data shown are means ± SE for n = 3 independent experiments.
Figure Legend Snippet: Ovarian cancer cells have differing levels of native resistance to cisplatin. Human OC cell lines SKOV3, OVCAR3, OV-90, 3AO and SKOV3 DDP were treated with increasing concentrations of cisplatin (0–500 umol/L) for 72 h. The viabilities indicated on the y axis were determined by MTT assays and normalized to control. Data shown are means ± SE for n = 3 independent experiments.

Techniques Used: MTT Assay

17) Product Images from "Bucillamine prevents cisplatin-induced ototoxicity through induction of glutathione and antioxidant genes"

Article Title: Bucillamine prevents cisplatin-induced ototoxicity through induction of glutathione and antioxidant genes

Journal: Experimental & Molecular Medicine

doi: 10.1038/emm.2014.112

Bucillamine scavenges ROS generated by cisplatin in HEI-OC1 cells. ( a ) To test spontaneous production of intracellular ROS, cells were treated with DCF-DA, a ROS-specific fluorescence dye, for 1 h and then, fluorescence intensity was measured using a flow cytometer. ( b ) Cells were pretreated with 2 m M bucillamine followed by the addition of 20 μ M cisplatin for 24 h. Then, cells were incubated with the dyes, including DCF-DA for hydroxyl radical and 4-amino-5-methylamino-2′,7′-difluorofluorescein for nitric oxides. After 1 h, the fluorescence intensity was measured using a flow cytometer. ( c ) Relative intensities from FACS analyses are shown in the bar graph.
Figure Legend Snippet: Bucillamine scavenges ROS generated by cisplatin in HEI-OC1 cells. ( a ) To test spontaneous production of intracellular ROS, cells were treated with DCF-DA, a ROS-specific fluorescence dye, for 1 h and then, fluorescence intensity was measured using a flow cytometer. ( b ) Cells were pretreated with 2 m M bucillamine followed by the addition of 20 μ M cisplatin for 24 h. Then, cells were incubated with the dyes, including DCF-DA for hydroxyl radical and 4-amino-5-methylamino-2′,7′-difluorofluorescein for nitric oxides. After 1 h, the fluorescence intensity was measured using a flow cytometer. ( c ) Relative intensities from FACS analyses are shown in the bar graph.

Techniques Used: Generated, Fluorescence, Flow Cytometry, Cytometry, Incubation, FACS

Bucillamine induces the subcellular localization of Nrf2 in HEI-OC1 cells treated with cisplatin. ( a ) Cells grown in chamber slides were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 12 h. Subcellular localization of Nrf2 was detected by indirect immunofluorescence staining with anti-Nrf2 antibodies followed by Alexa488–conjugated second antibodies (green). The nucleus (left panel) was stained with DAPI (blue), and fluorescent images were obtained. ( b ) Cytosolic (CE) and nuclear (NE) extracts from cells were separated on 12% SDS-PAGE and subjected to western blot analysis using anti-Nrf2 antibody. ( c ) Quantitative real-time PCR was carried out to determine the relative expression level of Nrf2 at 3 h. ( d ) Total RNA from cells was isolated with TRIzol reagent, cDNA was generated using reverse transcriptase, and PCR was performed to determine expression levels of Nrf2 at indicated time points.
Figure Legend Snippet: Bucillamine induces the subcellular localization of Nrf2 in HEI-OC1 cells treated with cisplatin. ( a ) Cells grown in chamber slides were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 12 h. Subcellular localization of Nrf2 was detected by indirect immunofluorescence staining with anti-Nrf2 antibodies followed by Alexa488–conjugated second antibodies (green). The nucleus (left panel) was stained with DAPI (blue), and fluorescent images were obtained. ( b ) Cytosolic (CE) and nuclear (NE) extracts from cells were separated on 12% SDS-PAGE and subjected to western blot analysis using anti-Nrf2 antibody. ( c ) Quantitative real-time PCR was carried out to determine the relative expression level of Nrf2 at 3 h. ( d ) Total RNA from cells was isolated with TRIzol reagent, cDNA was generated using reverse transcriptase, and PCR was performed to determine expression levels of Nrf2 at indicated time points.

Techniques Used: Immunofluorescence, Staining, SDS Page, Western Blot, Real-time Polymerase Chain Reaction, Expressing, Isolation, Generated, Polymerase Chain Reaction

Bucillamine suppresses the catalytic activation of caspase-3 and caspase-8 in HEI-OC1 cells treated with cisplatin. Cells were pretreated with 2 m M bucillamine for 1 h, followed by the addition of 20 μ M cisplatin for 24 h. Cells lysates were reacted with Ac-IETD-pNA and Ac-DEVD-pNA, the p-NA-conjugated specific substrates for caspase-3 ( a ) and caspase-8 ( b ), respectively. Enzymatic activity assays for caspases were performed according to colorimetric assay at 405 nm absorbance using a spectrophotometer. Data are shown as the mean (s.d.) of triplicate experiments. * P
Figure Legend Snippet: Bucillamine suppresses the catalytic activation of caspase-3 and caspase-8 in HEI-OC1 cells treated with cisplatin. Cells were pretreated with 2 m M bucillamine for 1 h, followed by the addition of 20 μ M cisplatin for 24 h. Cells lysates were reacted with Ac-IETD-pNA and Ac-DEVD-pNA, the p-NA-conjugated specific substrates for caspase-3 ( a ) and caspase-8 ( b ), respectively. Enzymatic activity assays for caspases were performed according to colorimetric assay at 405 nm absorbance using a spectrophotometer. Data are shown as the mean (s.d.) of triplicate experiments. * P

Techniques Used: Activation Assay, Activity Assay, Colorimetric Assay, Spectrophotometry

Bucillamine protects sensory hair cells from cisplatin in rat primary organ of Corti explants and prevents hearing loss in adult mice. ( a ) Organ of Corti explants were dissected into three parts—basal, middle and apex turns—and treated with 20 μ M cisplatin alone, 2 m M bucillamine or cisplatin for 30 h. Cultures were stained with tetramethylrhodamine isothiocyanate-conjugated phalloidin and then observed under a fluorescence microscope. ( b ) Auditory-brainstem-evoked response (ABR) thresholds were measured 3 days after i.p. injection of cisplatin only (back bar, n =5), cisplatin plus bucillamine (hatch bar, n =5), bucillamine only (dot bar, n =5) and control (saline) only (white bar, n =5). ( c ) Click thresholds were measured using the same mice groups in ( b ). ABR threshold changes were compared with the basal level in the control mice injected with saline. Values are shown as the mean±s.e.m. * Indicates significant ( P
Figure Legend Snippet: Bucillamine protects sensory hair cells from cisplatin in rat primary organ of Corti explants and prevents hearing loss in adult mice. ( a ) Organ of Corti explants were dissected into three parts—basal, middle and apex turns—and treated with 20 μ M cisplatin alone, 2 m M bucillamine or cisplatin for 30 h. Cultures were stained with tetramethylrhodamine isothiocyanate-conjugated phalloidin and then observed under a fluorescence microscope. ( b ) Auditory-brainstem-evoked response (ABR) thresholds were measured 3 days after i.p. injection of cisplatin only (back bar, n =5), cisplatin plus bucillamine (hatch bar, n =5), bucillamine only (dot bar, n =5) and control (saline) only (white bar, n =5). ( c ) Click thresholds were measured using the same mice groups in ( b ). ABR threshold changes were compared with the basal level in the control mice injected with saline. Values are shown as the mean±s.e.m. * Indicates significant ( P

Techniques Used: Mouse Assay, Staining, Fluorescence, Microscopy, Injection

Bucillamine induces phase II antioxidants and detoxifying enzymes in HEI-OC1 cells treated with cisplatin. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin at 12 h. Phase II antioxidant genes ( HO-1 , SOD1 and SOD2 ) from total RNA were amplified using specific primer sets. Expression levels of HO-1, SOD1 and SOD2 were significantly increased by the pretreatment with bucillamine as compared with cisplatin alone at 12 h. ( b ) Cell lysates were electrophoresed through an SDS-polyacrylamide gel and subject to immunoblot analysis for HO-1, SOD1 and SOD2.
Figure Legend Snippet: Bucillamine induces phase II antioxidants and detoxifying enzymes in HEI-OC1 cells treated with cisplatin. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin at 12 h. Phase II antioxidant genes ( HO-1 , SOD1 and SOD2 ) from total RNA were amplified using specific primer sets. Expression levels of HO-1, SOD1 and SOD2 were significantly increased by the pretreatment with bucillamine as compared with cisplatin alone at 12 h. ( b ) Cell lysates were electrophoresed through an SDS-polyacrylamide gel and subject to immunoblot analysis for HO-1, SOD1 and SOD2.

Techniques Used: Amplification, Expressing

siRNA knockdown of HO-1 and SOD2 enzymes does not completely block the protective effects of bucillamine. ( a ) After transfection of HEI-OC1 cell with double-stranded siRNA (HO-1, SOD2 or both), cells were pretreated with various concentrations of bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 24 h. Then, cell viability was measured by MTT assays. ( b ) Cell lysates were subject to immunoblot analysis with antibodies against pro-caspase-3 and active form of caspase-3. β-actin was used as a control.
Figure Legend Snippet: siRNA knockdown of HO-1 and SOD2 enzymes does not completely block the protective effects of bucillamine. ( a ) After transfection of HEI-OC1 cell with double-stranded siRNA (HO-1, SOD2 or both), cells were pretreated with various concentrations of bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 24 h. Then, cell viability was measured by MTT assays. ( b ) Cell lysates were subject to immunoblot analysis with antibodies against pro-caspase-3 and active form of caspase-3. β-actin was used as a control.

Techniques Used: Blocking Assay, Transfection, MTT Assay

Bucillamine suppresses cisplatin-induced caspase-3 activation in HEI-OC1 cells. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 24 h. Cells were then washed and fixed, and the active form of caspase-3 was determined by immunofluorescence. Pictures were taken using a fluorescence microscope (original magnification, × 600). ( b ) Equal amounts of total proteins (50 μg per lane) from cell lysate of the above experimental conditions were prepared, and subject to SDS-PAGE and western blot analyses.
Figure Legend Snippet: Bucillamine suppresses cisplatin-induced caspase-3 activation in HEI-OC1 cells. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 24 h. Cells were then washed and fixed, and the active form of caspase-3 was determined by immunofluorescence. Pictures were taken using a fluorescence microscope (original magnification, × 600). ( b ) Equal amounts of total proteins (50 μg per lane) from cell lysate of the above experimental conditions were prepared, and subject to SDS-PAGE and western blot analyses.

Techniques Used: Activation Assay, Immunofluorescence, Fluorescence, Microscopy, SDS Page, Western Blot

Pretreatment with bucillamine protects HEI-OC1 cells from cisplatin-induced apoptosis. ( a ) Cells were pretreated with various concentrations of bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 30 h, and cell viability was measured by MTT assays. ( b ) Genomic DNA isolated from cells, treated as indicated, was subject to 1.5% agarose gel electrophoresis. ( c ) Cells were stained with DAPI and observed under a fluorescence microscope to detect morphological changes in the nuclei. ( d ) Cells were treated with 2 m M bucillamine and the cell cycle was analyzed, according to sub-G 0 /G 1 fraction ratio by flow cytometry. The results are shown as the mean % (s.d.) of triplicate experiments. * Indicates a significant difference between cells treated with medium alone, cisplatin or cisplatin plus bucillamine ( P
Figure Legend Snippet: Pretreatment with bucillamine protects HEI-OC1 cells from cisplatin-induced apoptosis. ( a ) Cells were pretreated with various concentrations of bucillamine for 1 h followed by the addition of 20 μ M cisplatin for 30 h, and cell viability was measured by MTT assays. ( b ) Genomic DNA isolated from cells, treated as indicated, was subject to 1.5% agarose gel electrophoresis. ( c ) Cells were stained with DAPI and observed under a fluorescence microscope to detect morphological changes in the nuclei. ( d ) Cells were treated with 2 m M bucillamine and the cell cycle was analyzed, according to sub-G 0 /G 1 fraction ratio by flow cytometry. The results are shown as the mean % (s.d.) of triplicate experiments. * Indicates a significant difference between cells treated with medium alone, cisplatin or cisplatin plus bucillamine ( P

Techniques Used: MTT Assay, Isolation, Agarose Gel Electrophoresis, Staining, Fluorescence, Microscopy, Flow Cytometry, Cytometry

Bucillamine increases expression of γ-GCS and GSS in HEI-OC1 cells. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for different time intervals as indicated. Total RNA was isolated and cDNA was synthesized by reverse transcription. cDNAs of γ-glutamylcysteine synthetase (γ-GCS: GCLC and GCLM) and glutathione synthetase (GSS) were amplified using specific primer sets. ( b ) mRNA expression levels of GSS, GCLC and GCLM were analyzed by quantitative real-time PCR at 12 h. ( c ) Cell lysates were collected, electrophoresed through an SDS-polyacrylamide gel, and subject to immunoblot analysis with antibodies against γ-GCS (GCLC and GCLM) or GSS. The protein and mRNA levels of β-actin were used as controls. ( d ) Intracellular GSH content was measured by using a Glutathione Assay Kit. Total GSH contents were expressed as nmol mg −1 protein. Values are represented as the mean (s.d.) of triplicate samples. * P
Figure Legend Snippet: Bucillamine increases expression of γ-GCS and GSS in HEI-OC1 cells. ( a ) Cells were pretreated with 2 m M bucillamine for 1 h followed by the addition of 20 μ M cisplatin for different time intervals as indicated. Total RNA was isolated and cDNA was synthesized by reverse transcription. cDNAs of γ-glutamylcysteine synthetase (γ-GCS: GCLC and GCLM) and glutathione synthetase (GSS) were amplified using specific primer sets. ( b ) mRNA expression levels of GSS, GCLC and GCLM were analyzed by quantitative real-time PCR at 12 h. ( c ) Cell lysates were collected, electrophoresed through an SDS-polyacrylamide gel, and subject to immunoblot analysis with antibodies against γ-GCS (GCLC and GCLM) or GSS. The protein and mRNA levels of β-actin were used as controls. ( d ) Intracellular GSH content was measured by using a Glutathione Assay Kit. Total GSH contents were expressed as nmol mg −1 protein. Values are represented as the mean (s.d.) of triplicate samples. * P

Techniques Used: Expressing, Isolation, Synthesized, Amplification, Real-time Polymerase Chain Reaction, Glutathione Assay

18) Product Images from "Protective effects of ethyl pyruvate in cisplatin-induced nephrotoxicity"

Article Title: Protective effects of ethyl pyruvate in cisplatin-induced nephrotoxicity

Journal: Biotechnology, Biotechnological Equipment

doi: 10.1080/13102818.2014.942489

Photomicrographs of hematoxylin and eosin stained sections of kidney of rats (kidney histology magnification 200×). Typical features of normal histological appearence of the corticomedullary region of rat kidney sections are observed in control and EP administered groups (A, B). In kidney sections of cisplatin pretreated rats, marked changes were observed in tubulus and glomerule structures. In some corticomedullary regions focal tubular necrosis (big solid arrows), haemorrhagia (small letter h) and dilatation (small letter d) as well as inflammatory cell infiltration (small hollow triangle) in the intersititium can be seen. Furthermore, necrotic cell debris and vacuolization (arrow heads) in tubulus epithelium and protein casts in tubular lumina are evident (C, E). The sections obtained from the cisplatin + EP group are found almost similar to that of those in the control group. Rare inflammatory cell infiltration, minimal (asteriks symbols) tubular dilatation and vacuolization images can be seen. It is considered that the renal injury induced by cisplatin is prevented to a great extent by EP co-administration (D, F).
Figure Legend Snippet: Photomicrographs of hematoxylin and eosin stained sections of kidney of rats (kidney histology magnification 200×). Typical features of normal histological appearence of the corticomedullary region of rat kidney sections are observed in control and EP administered groups (A, B). In kidney sections of cisplatin pretreated rats, marked changes were observed in tubulus and glomerule structures. In some corticomedullary regions focal tubular necrosis (big solid arrows), haemorrhagia (small letter h) and dilatation (small letter d) as well as inflammatory cell infiltration (small hollow triangle) in the intersititium can be seen. Furthermore, necrotic cell debris and vacuolization (arrow heads) in tubulus epithelium and protein casts in tubular lumina are evident (C, E). The sections obtained from the cisplatin + EP group are found almost similar to that of those in the control group. Rare inflammatory cell infiltration, minimal (asteriks symbols) tubular dilatation and vacuolization images can be seen. It is considered that the renal injury induced by cisplatin is prevented to a great extent by EP co-administration (D, F).

Techniques Used: Staining

19) Product Images from "The Potential Role of Azadirachta indica Treatment on Cisplatin-Induced Hepatotoxicity and Oxidative Stress in Female Rats"

Article Title: The Potential Role of Azadirachta indica Treatment on Cisplatin-Induced Hepatotoxicity and Oxidative Stress in Female Rats

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2013/741817

Protective effects of neem leaves extract on cisplatin-induced reduction in superoxide dismutase and catalase activities in liver of rats. Values are means ± SEM ( n = 6). a P
Figure Legend Snippet: Protective effects of neem leaves extract on cisplatin-induced reduction in superoxide dismutase and catalase activities in liver of rats. Values are means ± SEM ( n = 6). a P

Techniques Used:

NF- κ B expression changes in the liver of rats. (a) Normal liver showing very weak expression for NF- κ B. (b) Treated liver with cisplatin showing positive expression for NF- κ B. (c) Neem treated liver showing negative expression for NF- κ B. (d) Treated liver with cisplatin and MNLE showing medium expression for NF- κ B (400x).
Figure Legend Snippet: NF- κ B expression changes in the liver of rats. (a) Normal liver showing very weak expression for NF- κ B. (b) Treated liver with cisplatin showing positive expression for NF- κ B. (c) Neem treated liver showing negative expression for NF- κ B. (d) Treated liver with cisplatin and MNLE showing medium expression for NF- κ B (400x).

Techniques Used: Expressing

Relative quantification using RT-qPCR of mRNA expression of caspase-3, 9, and Bax genes in liver of rats treated with cisplatin and neem leaves extract. a P
Figure Legend Snippet: Relative quantification using RT-qPCR of mRNA expression of caspase-3, 9, and Bax genes in liver of rats treated with cisplatin and neem leaves extract. a P

Techniques Used: Quantitative RT-PCR, Expressing

Histological changes in the liver of rats. (a) A control liver with normal architecture. (b) Rats treated with cisplatin with prominent inflammation and hepatocytic vacuolation. (c) Rats treated with the neem leaves extract for 5 days. (d) Rats treated with the cisplatin and neem leaves extract. Sections were stained with hematoxylin and eosin (400x).
Figure Legend Snippet: Histological changes in the liver of rats. (a) A control liver with normal architecture. (b) Rats treated with cisplatin with prominent inflammation and hepatocytic vacuolation. (c) Rats treated with the neem leaves extract for 5 days. (d) Rats treated with the cisplatin and neem leaves extract. Sections were stained with hematoxylin and eosin (400x).

Techniques Used: Staining

Protective effects of neem leaves extract on cisplatin-induced elevation in lipid peroxidation, nitric oxide levels, and reduction in glutathione level in liver of rats. Values are means ± SEM ( n = 6). a P
Figure Legend Snippet: Protective effects of neem leaves extract on cisplatin-induced elevation in lipid peroxidation, nitric oxide levels, and reduction in glutathione level in liver of rats. Values are means ± SEM ( n = 6). a P

Techniques Used:

20) Product Images from "Protective effects of the Morus alba L. leaf extracts on cisplatin-induced nephrotoxicity in rat"

Article Title: Protective effects of the Morus alba L. leaf extracts on cisplatin-induced nephrotoxicity in rat

Journal: Research in Pharmaceutical Sciences

doi:

Effect of different doses of hydroalcoholic extract of M. alba on serum BUN concentration in cisplatin-treated rats. Normal group received normal saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received hydroalcoholic extract (200, 400 and 600 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum Blood urea nitrogen (BUN) concentration of 7-9 animals in each group. MAHE; M. alba hydroalcoholic extract.
Figure Legend Snippet: Effect of different doses of hydroalcoholic extract of M. alba on serum BUN concentration in cisplatin-treated rats. Normal group received normal saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received hydroalcoholic extract (200, 400 and 600 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum Blood urea nitrogen (BUN) concentration of 7-9 animals in each group. MAHE; M. alba hydroalcoholic extract.

Techniques Used: Concentration Assay, Injection

Effect of different doses of hydroalcoholic extract of M. alba on serum creatinine concentration in cisplatin-treated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received hydroalcoholic extract (200, 400 and 600 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum creatinine concentration of 7-9 animals in each group. MAHE; M. alba hydroalcoholic extract.
Figure Legend Snippet: Effect of different doses of hydroalcoholic extract of M. alba on serum creatinine concentration in cisplatin-treated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received hydroalcoholic extract (200, 400 and 600 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum creatinine concentration of 7-9 animals in each group. MAHE; M. alba hydroalcoholic extract.

Techniques Used: Concentration Assay, Injection

Effect of different doses of flavonoid fraction of M. alba on serum BUN concentration in cisplatintreated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received flavonoid fraction (50, 100 and 200 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum BUN concentration of 7-9 animals in each group. MAFF; M. alba flavonoid fraction. * P
Figure Legend Snippet: Effect of different doses of flavonoid fraction of M. alba on serum BUN concentration in cisplatintreated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7 mg/kg, i.p) was injected. Other groups received flavonoid fraction (50, 100 and 200 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum BUN concentration of 7-9 animals in each group. MAFF; M. alba flavonoid fraction. * P

Techniques Used: Concentration Assay, Injection

Effect of different doses of flavonoid fraction of M. alba on serum creatinine concentration in cisplatintreated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7mg/kg, i.p) was injected. Other groups received flavonoid fraction (50, 100 and 200 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum creatinine concentration of 7-9 animals in each group. MAFF; M. alba flavonoid fraction. P
Figure Legend Snippet: Effect of different doses of flavonoid fraction of M. alba on serum creatinine concentration in cisplatintreated rats. Normal group received saline (0.2 ml, i.p.) once daily for 10 days. Control group received saline (0.2 ml, i.p.) for 2 days and in the third day cisplatin (7mg/kg, i.p) was injected. Other groups received flavonoid fraction (50, 100 and 200 mg/kg, i.p.) for two days before cisplatin administration and thereafter until tenth day. Data represent mean ± S.E.M of serum creatinine concentration of 7-9 animals in each group. MAFF; M. alba flavonoid fraction. P

Techniques Used: Concentration Assay, Injection

Effect of M. alba polyphenolic extract on the kidney histological changes induced by cisplatin in rat. A: normal group; B: cisplatin-treated group; C: M. alba flavonoid fraction (100 mg/kg) + cisplatin; D: M. alba flavonoid fraction (200 mg/kg) + cisplatin. Cisplatin treatment was associated with a loss of tubular architecture, and the integrity and hypercellularity of the interstitium (panel B). In contrast, M. alba flavonoid fraction prevented the damage (C and D).
Figure Legend Snippet: Effect of M. alba polyphenolic extract on the kidney histological changes induced by cisplatin in rat. A: normal group; B: cisplatin-treated group; C: M. alba flavonoid fraction (100 mg/kg) + cisplatin; D: M. alba flavonoid fraction (200 mg/kg) + cisplatin. Cisplatin treatment was associated with a loss of tubular architecture, and the integrity and hypercellularity of the interstitium (panel B). In contrast, M. alba flavonoid fraction prevented the damage (C and D).

Techniques Used:

21) Product Images from "Elevated Expression of the Serine-Arginine Protein Kinase 1 Gene in Ovarian Cancer and Its Role in Cisplatin Cytotoxicity In Vitro"

Article Title: Elevated Expression of the Serine-Arginine Protein Kinase 1 Gene in Ovarian Cancer and Its Role in Cisplatin Cytotoxicity In Vitro

Journal: PLoS ONE

doi: 10.1371/journal.pone.0051030

Forced inhibition of SRPK1 expression in ovarian cancer cell lines enhances sensitivity to cisplatin. Ovarian cancer cells were transiently (A) or stably (C) transfected with either the siRNA-encoding shSRPK1 plasmid or the empty vector (pSM2-EV). Protein levels of SRPK1, UPF1 and actin were determined by Western blot analysis. Representative blots from three independent experiments are shown. (B) and (D) SRPK1 knockdown enhances cisplatin cytotoxicity. (B) Cells (5×10 4 ) were reseeded 24 h after transfection, treated with various concentrations of cisplatin for 48 hr and the number of surviving cells was analyzed by MTT assay. Survival (%) is expressed relative to non-treated pSM2-EV cells. (D) Stable transfectants (3×10 2 ) were seeded in triplicate, treated with cisplatin for 24 hr and colony formation was assessed after 10–14 days. Data were analyzed with one way ANOVA and * indicates P
Figure Legend Snippet: Forced inhibition of SRPK1 expression in ovarian cancer cell lines enhances sensitivity to cisplatin. Ovarian cancer cells were transiently (A) or stably (C) transfected with either the siRNA-encoding shSRPK1 plasmid or the empty vector (pSM2-EV). Protein levels of SRPK1, UPF1 and actin were determined by Western blot analysis. Representative blots from three independent experiments are shown. (B) and (D) SRPK1 knockdown enhances cisplatin cytotoxicity. (B) Cells (5×10 4 ) were reseeded 24 h after transfection, treated with various concentrations of cisplatin for 48 hr and the number of surviving cells was analyzed by MTT assay. Survival (%) is expressed relative to non-treated pSM2-EV cells. (D) Stable transfectants (3×10 2 ) were seeded in triplicate, treated with cisplatin for 24 hr and colony formation was assessed after 10–14 days. Data were analyzed with one way ANOVA and * indicates P

Techniques Used: Inhibition, Expressing, Stable Transfection, Transfection, Plasmid Preparation, Western Blot, MTT Assay

22) Product Images from "Sodium arsenite and hyperthermia modulate cisplatin-DNA damage responses and enhance platinum accumulation in murine metastatic ovarian cancer xenograft after hyperthermic intraperitoneal chemotherapy (HIPEC)"

Article Title: Sodium arsenite and hyperthermia modulate cisplatin-DNA damage responses and enhance platinum accumulation in murine metastatic ovarian cancer xenograft after hyperthermic intraperitoneal chemotherapy (HIPEC)

Journal: Journal of Ovarian Research

doi: 10.1186/1757-2215-4-9

Immunocytochemical determination of p53, XPA and MSH2 expression in ovarian cancer cells . A. A2780/CP70 cells were treated for 1 h with 40 μM cisplatin. Cells were washed and incubated in drug-free media for 24 h and immunohistochemistry was performed. Representative pictures of cells at 20x magnification for secondary antibody only control (a), p53 (b), XPA (c) and MSH2 (d). B. Plot of 3,3'-diaminobenzidine (DAB)-positive cells. Data are single biological experiment performed in duplicate slides. Four different fields were counted per coverslip.
Figure Legend Snippet: Immunocytochemical determination of p53, XPA and MSH2 expression in ovarian cancer cells . A. A2780/CP70 cells were treated for 1 h with 40 μM cisplatin. Cells were washed and incubated in drug-free media for 24 h and immunohistochemistry was performed. Representative pictures of cells at 20x magnification for secondary antibody only control (a), p53 (b), XPA (c) and MSH2 (d). B. Plot of 3,3'-diaminobenzidine (DAB)-positive cells. Data are single biological experiment performed in duplicate slides. Four different fields were counted per coverslip.

Techniques Used: Expressing, Incubation, Immunohistochemistry

Murine hyperthermic intraperitoneal chemotherapy model . A. Drawing of tumor bearing mouse undergoing HIPEC. Depicted are inlet (a) and outlet (b) ports and anal temperature probe (c) to monitor internal temperature of mouse during perfusion. B. Photograph showing perfusion pump (a), temperature monitor (b), flow tubes (c) and heating bath (d). Mice were perfused for 1 h at the rate of 3 mL/min with cisplatin (3 mg/kg) ± NaAsO 2 (26 mg/kg) at 37 or 43°C.
Figure Legend Snippet: Murine hyperthermic intraperitoneal chemotherapy model . A. Drawing of tumor bearing mouse undergoing HIPEC. Depicted are inlet (a) and outlet (b) ports and anal temperature probe (c) to monitor internal temperature of mouse during perfusion. B. Photograph showing perfusion pump (a), temperature monitor (b), flow tubes (c) and heating bath (d). Mice were perfused for 1 h at the rate of 3 mL/min with cisplatin (3 mg/kg) ± NaAsO 2 (26 mg/kg) at 37 or 43°C.

Techniques Used: Flow Cytometry, Mouse Assay

Inductively Coupled Plasma Mass Spectrometry (ICP-MS) determination of platinum and arsenic in tumors . Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin + NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tumors from untreated (UT) and treated mice were harvested at 0 and 24 h after treatment. Tumors were homogenized and samples of the homogenate were analyzed for protein concentration by BCA or digested in nitric acid for ICP-MS analysis for platinum and arsenic. Data are presented as means ± SEM of ≥3 tumors each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P
Figure Legend Snippet: Inductively Coupled Plasma Mass Spectrometry (ICP-MS) determination of platinum and arsenic in tumors . Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin + NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tumors from untreated (UT) and treated mice were harvested at 0 and 24 h after treatment. Tumors were homogenized and samples of the homogenate were analyzed for protein concentration by BCA or digested in nitric acid for ICP-MS analysis for platinum and arsenic. Data are presented as means ± SEM of ≥3 tumors each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P

Techniques Used: Mass Spectrometry, Mouse Assay, Protein Concentration, BIA-KA

DNA repair protein expression in tumors . A. Western blot determination of p53, XPC, XPA, ERCC1 and MSH2 in tumors. GAPDH is loading control. B . Densitometry analyses of ( a ) p53, ( b ) XPC, ( c ) XPA, ( d ) ERCC1 and ( e ) MSH2 normalized to GAPDH loading control and untreated tumors. Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin plus NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tumors from untreated (UT) mice and treated mice were harvested 0 and 24 h after treatment. Protein extracts were prepared from the tumors and 20 μg loaded per lane for SDS-PAGE. Data are presented as means ± SD of ≥5 tumors each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P
Figure Legend Snippet: DNA repair protein expression in tumors . A. Western blot determination of p53, XPC, XPA, ERCC1 and MSH2 in tumors. GAPDH is loading control. B . Densitometry analyses of ( a ) p53, ( b ) XPC, ( c ) XPA, ( d ) ERCC1 and ( e ) MSH2 normalized to GAPDH loading control and untreated tumors. Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin plus NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tumors from untreated (UT) mice and treated mice were harvested 0 and 24 h after treatment. Protein extracts were prepared from the tumors and 20 μg loaded per lane for SDS-PAGE. Data are presented as means ± SD of ≥5 tumors each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P

Techniques Used: Expressing, Western Blot, Mouse Assay, SDS Page

Platinum and arsenic accumulation in somatic tissues . Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin + NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tissues from untreated (UT) and treated mice were harvested at 0 and 24 h after treatment. Tissue samples were weighed and digested in nitric acid for ICP-MS analysis for platinum ( A ) and arsenic ( B ). Data are presented as means ± SD of triplicate samples each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P
Figure Legend Snippet: Platinum and arsenic accumulation in somatic tissues . Mice were perfused for 1 h with cisplatin (CP/37; CP/43) or cisplatin + NaAsO 2 (CPA/37; CPA/43) at 37 or 43°C respectively. Tissues from untreated (UT) and treated mice were harvested at 0 and 24 h after treatment. Tissue samples were weighed and digested in nitric acid for ICP-MS analysis for platinum ( A ) and arsenic ( B ). Data are presented as means ± SD of triplicate samples each from different mice. Statistical analysis was performed using wilcoxon rank sum test. P

Techniques Used: Mouse Assay, Mass Spectrometry

23) Product Images from "Concordant and opposite roles of DNA-PK and the "facilitator of chromatin transcription" (FACT) in DNA repair, apoptosis and necrosis after cisplatin"

Article Title: Concordant and opposite roles of DNA-PK and the "facilitator of chromatin transcription" (FACT) in DNA repair, apoptosis and necrosis after cisplatin

Journal: Molecular Cancer

doi: 10.1186/1476-4598-10-74

Cisplatin-induced recruitment of FACT to the Ku complex . A. Purification of the Ku86 complex. Tandem affinity purification for FLAG and HA was performed on nuclear extracts from S3 or S3-Ku86-Flag/HA cells 0, 1, 2 and 4 hours (hrs) after cisplatin (CIS) treatment. The purified complexes were resolved by 4-12% NuPAGE and visualized by silver staining. Arrows show Ku70, Ku86-Flag/HA, the band identified as spt16 through MSMS analysis and DNA-PKcs (based on molecular weight). The molecular weight markers are indicated on the left (in kDa). B. Association of FACT with the Ku complex. Complexes purified as in (A) before or 4 hrs after cisplatin treatment (+CIS) were immunoblotted for the indicated proteins. Cells were pre-treated with the DNA-PK inhibitor Nu7026 as indicated. C. Cisplatin-induced association of γH2AX with the Ku complex. Inputs are nuclear extracts (NEX) and chromatin obtained before or 4 hrs after cisplatin treatment (+CIS). Inputs and Ku86 complexes purified from the inputs were immunoblotted for the indicated proteins. D. Treatment of the Ku complex with DNase reveals DNA-dependent interactions. Ku86 complexes were purified as in (A) 2 hrs after cisplatin treatment. The complexes immobilized on anti-HA beads were left untreated or treated with DNase and then eluted with the HA peptide. The resulting complexes were analyzed by immunoblotting for the indicated proteins.
Figure Legend Snippet: Cisplatin-induced recruitment of FACT to the Ku complex . A. Purification of the Ku86 complex. Tandem affinity purification for FLAG and HA was performed on nuclear extracts from S3 or S3-Ku86-Flag/HA cells 0, 1, 2 and 4 hours (hrs) after cisplatin (CIS) treatment. The purified complexes were resolved by 4-12% NuPAGE and visualized by silver staining. Arrows show Ku70, Ku86-Flag/HA, the band identified as spt16 through MSMS analysis and DNA-PKcs (based on molecular weight). The molecular weight markers are indicated on the left (in kDa). B. Association of FACT with the Ku complex. Complexes purified as in (A) before or 4 hrs after cisplatin treatment (+CIS) were immunoblotted for the indicated proteins. Cells were pre-treated with the DNA-PK inhibitor Nu7026 as indicated. C. Cisplatin-induced association of γH2AX with the Ku complex. Inputs are nuclear extracts (NEX) and chromatin obtained before or 4 hrs after cisplatin treatment (+CIS). Inputs and Ku86 complexes purified from the inputs were immunoblotted for the indicated proteins. D. Treatment of the Ku complex with DNase reveals DNA-dependent interactions. Ku86 complexes were purified as in (A) 2 hrs after cisplatin treatment. The complexes immobilized on anti-HA beads were left untreated or treated with DNase and then eluted with the HA peptide. The resulting complexes were analyzed by immunoblotting for the indicated proteins.

Techniques Used: Purification, Affinity Purification, Silver Staining, Molecular Weight

Differential regulation of cisplatin-induced apoptosis and necrosis by DNA-PK and FACT . A. Regulation of cisplatin-induced apoptosis and necrosis by DNA-PKcs. DNA-PKcs and control shRNA-expressing A2780 cells were treated with 25 μg/ml cisplatin for 24 hrs and relative amounts of nucleosomes were quantified in lysates (apoptosis) and culture supernatants (necrosis). Comparison between cisplatin treated control and DNA-PKcs depleted cells is shown, p
Figure Legend Snippet: Differential regulation of cisplatin-induced apoptosis and necrosis by DNA-PK and FACT . A. Regulation of cisplatin-induced apoptosis and necrosis by DNA-PKcs. DNA-PKcs and control shRNA-expressing A2780 cells were treated with 25 μg/ml cisplatin for 24 hrs and relative amounts of nucleosomes were quantified in lysates (apoptosis) and culture supernatants (necrosis). Comparison between cisplatin treated control and DNA-PKcs depleted cells is shown, p

Techniques Used: shRNA, Expressing

Dual role of DNA-PK in response to cisplatin . A. Cisplatin-induced phosphorylation of H2AX is regulated by DNA-PK. DNA-PKcs (PKcs) or control (ctr) shRNA-expressing A2780 cells were treated with 100 μg/ml cisplatin (CIS) for 0, 1 or 2 hours (hrs). DNA-PKcs and β-actin were analyzed in whole cell lysates by immunoblotting. γH2AX and H2A were analyzed in chromatin fractions (chrom). B. Levels of cisplatin-induced PARP-1 cleavage after silencing DNA-PKcs expression in A2780 cells. DNA-PKcs, PARP-1, and β-actin were analyzed in whole cell lysates of cells treated with 100 μg/ml cisplatin for 0, 4 or 6 hrs by immunoblotting. C. DNA-PK inhibition sensitizes cancer cells to cisplatin. Control and DNA-PKcs shRNA-expressing A2780, MDA-MB-231 and HEK293T cells were treated with increasing concentrations of cisplatin. IC 50 values at 24 hrs are shown. Results represent the mean ± s.e.m. of five independent experiments. For comparisons of control and DNA-PKcs depletion within cell lines, p
Figure Legend Snippet: Dual role of DNA-PK in response to cisplatin . A. Cisplatin-induced phosphorylation of H2AX is regulated by DNA-PK. DNA-PKcs (PKcs) or control (ctr) shRNA-expressing A2780 cells were treated with 100 μg/ml cisplatin (CIS) for 0, 1 or 2 hours (hrs). DNA-PKcs and β-actin were analyzed in whole cell lysates by immunoblotting. γH2AX and H2A were analyzed in chromatin fractions (chrom). B. Levels of cisplatin-induced PARP-1 cleavage after silencing DNA-PKcs expression in A2780 cells. DNA-PKcs, PARP-1, and β-actin were analyzed in whole cell lysates of cells treated with 100 μg/ml cisplatin for 0, 4 or 6 hrs by immunoblotting. C. DNA-PK inhibition sensitizes cancer cells to cisplatin. Control and DNA-PKcs shRNA-expressing A2780, MDA-MB-231 and HEK293T cells were treated with increasing concentrations of cisplatin. IC 50 values at 24 hrs are shown. Results represent the mean ± s.e.m. of five independent experiments. For comparisons of control and DNA-PKcs depletion within cell lines, p

Techniques Used: shRNA, Expressing, Inhibition, Multiple Displacement Amplification

Role of FACT in response to cisplatin . A. Cisplatin-induced appearance γH2AX is SSRP1-dependent. SSRP1 or control (ctr) shRNA-expressing A2780 cells were treated with 100 μg/ml cisplatin for 0, 1 or 2 hrs. Using immunoblotting SSRP1 and β-actin were detected in whole cell lysates and γH2AX and H2A in chromatin fractions. B. FACT inhibition sensitizes cancer cells to cisplatin. SSRP1 and control shRNA-expressing A2780, MDA-MB-231 and HEK293T cells were treated with increasing concentrations of cisplatin. IC 50 values at 24 hrs are shown. Results represent the mean ± s.e.m. of five independent experiments. For comparisons of control and SSRP1 depletion within cell lines, p
Figure Legend Snippet: Role of FACT in response to cisplatin . A. Cisplatin-induced appearance γH2AX is SSRP1-dependent. SSRP1 or control (ctr) shRNA-expressing A2780 cells were treated with 100 μg/ml cisplatin for 0, 1 or 2 hrs. Using immunoblotting SSRP1 and β-actin were detected in whole cell lysates and γH2AX and H2A in chromatin fractions. B. FACT inhibition sensitizes cancer cells to cisplatin. SSRP1 and control shRNA-expressing A2780, MDA-MB-231 and HEK293T cells were treated with increasing concentrations of cisplatin. IC 50 values at 24 hrs are shown. Results represent the mean ± s.e.m. of five independent experiments. For comparisons of control and SSRP1 depletion within cell lines, p

Techniques Used: shRNA, Expressing, Inhibition, Multiple Displacement Amplification

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    Millipore cisplatin
    Morphological analysis ( A ) and cell death induction studies ( B ); ( A ) TEM analysis of HCT-15 colon cancer cells: ( a , b ) control cells; ( c , d ) HCT-15 cells treated for 24 h with IC 50 concentrations of 4 ; ( e , f ) HCT-15 cells treated for 24 h with IC 50 concentrations of 8 ; ( B ) Hoechst staining of HCT-15 cells: ( a ) control cells; HCT-15 cells incubated for 24 or 48 h with IC 50 doses of 4 ( b , c ), 8 ( d , e ), or <t>cisplatin</t> ( f , g ).
    Cisplatin, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Morphological analysis ( A ) and cell death induction studies ( B ); ( A ) TEM analysis of HCT-15 colon cancer cells: ( a , b ) control cells; ( c , d ) HCT-15 cells treated for 24 h with IC 50 concentrations of 4 ; ( e , f ) HCT-15 cells treated for 24 h with IC 50 concentrations of 8 ; ( B ) Hoechst staining of HCT-15 cells: ( a ) control cells; HCT-15 cells incubated for 24 or 48 h with IC 50 doses of 4 ( b , c ), 8 ( d , e ), or cisplatin ( f , g ).

    Journal: International Journal of Molecular Sciences

    Article Title: Exploring the Antitumor Potential of Copper Complexes Based on Ester Derivatives of Bis(pyrazol-1-yl)acetate Ligands

    doi: 10.3390/ijms23169397

    Figure Lengend Snippet: Morphological analysis ( A ) and cell death induction studies ( B ); ( A ) TEM analysis of HCT-15 colon cancer cells: ( a , b ) control cells; ( c , d ) HCT-15 cells treated for 24 h with IC 50 concentrations of 4 ; ( e , f ) HCT-15 cells treated for 24 h with IC 50 concentrations of 8 ; ( B ) Hoechst staining of HCT-15 cells: ( a ) control cells; HCT-15 cells incubated for 24 or 48 h with IC 50 doses of 4 ( b , c ), 8 ( d , e ), or cisplatin ( f , g ).

    Article Snippet: Cisplatin (Sigma Chemical Co., St. Louis, MO, USA) (Sigma Chemical Co.) was dissolved in 0.9% sodium chloride solution.

    Techniques: Transmission Electron Microscopy, Staining, Incubation

    A nuclear staining assay demonstrated apoptosis presented with bright-blue fluorescence of Hoechst 33342 in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs) cultured with methanolic extract and isolated compounds 1 – 3 from Cymbidium ensifolium for 24 h. Cisplatin, a recommended anticancer drug, was used as a positive control. Notably, there were no detected necrosis cells stained with red fluorescence of propidium iodide (PI) in all treated cells.

    Journal: Molecules

    Article Title: Three New Dihydrophenanthrene Derivatives from Cymbidium ensifolium and Their Cytotoxicity against Cancer Cells

    doi: 10.3390/molecules27072222

    Figure Lengend Snippet: A nuclear staining assay demonstrated apoptosis presented with bright-blue fluorescence of Hoechst 33342 in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs) cultured with methanolic extract and isolated compounds 1 – 3 from Cymbidium ensifolium for 24 h. Cisplatin, a recommended anticancer drug, was used as a positive control. Notably, there were no detected necrosis cells stained with red fluorescence of propidium iodide (PI) in all treated cells.

    Article Snippet: When compared with cisplatin (Sigma-Aldrich Chemical, St. Louis, MO, USA), the higher anticancer potency of compound 1 was indicated with the lower % viability in MCF7 and CaCo2 cells.

    Techniques: Staining, Fluorescence, Cell Culture, Isolation, Positive Control

    The relationship between cytotoxicity and the concentration of dihydrophenanthrene derivatives ( 1 – 3 ) from Cymbidium ensifolium in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs). Cisplatin, a recommended anticancer drug, was used as a positive control. The data were presented as means ± standard error of the mean (SEM) from three independent experiments. * p

    Journal: Molecules

    Article Title: Three New Dihydrophenanthrene Derivatives from Cymbidium ensifolium and Their Cytotoxicity against Cancer Cells

    doi: 10.3390/molecules27072222

    Figure Lengend Snippet: The relationship between cytotoxicity and the concentration of dihydrophenanthrene derivatives ( 1 – 3 ) from Cymbidium ensifolium in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs). Cisplatin, a recommended anticancer drug, was used as a positive control. The data were presented as means ± standard error of the mean (SEM) from three independent experiments. * p

    Article Snippet: When compared with cisplatin (Sigma-Aldrich Chemical, St. Louis, MO, USA), the higher anticancer potency of compound 1 was indicated with the lower % viability in MCF7 and CaCo2 cells.

    Techniques: Concentration Assay, Positive Control

    The percent (%) apoptosis calculated from nuclear staining assay in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs) cultured with methanolic extract and isolated compounds 1 – 3 from Cymbidium ensifolium for 24 h. Cisplatin, a recommended anticancer drug, was used as a positive control. The data were presented as means ± standard error of the mean (SEM) from three independent experiments. * p

    Journal: Molecules

    Article Title: Three New Dihydrophenanthrene Derivatives from Cymbidium ensifolium and Their Cytotoxicity against Cancer Cells

    doi: 10.3390/molecules27072222

    Figure Lengend Snippet: The percent (%) apoptosis calculated from nuclear staining assay in ( a ) lung cancer H460, ( b ) breast cancer MCF7, ( c ) colon cancer CaCo 2 , and ( d ) dermal papilla cells (DPCs) cultured with methanolic extract and isolated compounds 1 – 3 from Cymbidium ensifolium for 24 h. Cisplatin, a recommended anticancer drug, was used as a positive control. The data were presented as means ± standard error of the mean (SEM) from three independent experiments. * p

    Article Snippet: When compared with cisplatin (Sigma-Aldrich Chemical, St. Louis, MO, USA), the higher anticancer potency of compound 1 was indicated with the lower % viability in MCF7 and CaCo2 cells.

    Techniques: Staining, Cell Culture, Isolation, Positive Control