Structured Review

Cusabio tnf α
Inflammatory response in the brain after TBI and the pathomechanism of the anti-inflammatory effect of XFZY. Following TBI, the mechanical injury-stimulated cell membrane releases arachidonic acid (AA), which is metabolized into prostaglandin E2 (PGE2) and prostacyclin (PGI2) by cyclooxygenase-2 (COX-2) and into leukotrienes (LTB 4 ) by 5-lipoxygenase (5-LO). The three inflammatory mediators initiate acute inflammation, including changes in blood flow, increased capillary permeability and inflammatory cell recruitment in the brain injury ambitus zone, including polymorphonuclear leukocytes (i.e., neutrophils) and monocytes. Excess prostaglandins and leukotrienes contribute to chronic inflammation. The neutrophils are activated to further release chemotactic factors, devour necrotic tissue and sterilize bacteria. The influx of monocytes and resident microglial cells develop into macrophages, which secrete pro-inflammatory factors (e.g., <t>TNF-α</t> and IL-1β) and consume foreign bodies, necrotic tissue or apoptotic cells (e.g., efferocytosis). XFZY significantly suppressed the increased levels of blood AA, TNF-α and IL-1β in brain tissue, indicating that XFZY possesses anti-inflammatory effects. To target the PI3K-AKT-mTOR signaling pathway, XFZY significantly reversed the elevated phosphorylation of AKT/mTOR in brain tissue post-TBI, as well as the downstream p70S6K, resulting in a reduced translation ratio of inflammatory factors and exerting anti-inflammatory effects.
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1) Product Images from "Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway"

Article Title: Xuefu Zhuyu decoction, a traditional Chinese medicine, provides neuroprotection in a rat model of traumatic brain injury via an anti-inflammatory pathway

Journal: Scientific Reports

doi: 10.1038/srep20040

Inflammatory response in the brain after TBI and the pathomechanism of the anti-inflammatory effect of XFZY. Following TBI, the mechanical injury-stimulated cell membrane releases arachidonic acid (AA), which is metabolized into prostaglandin E2 (PGE2) and prostacyclin (PGI2) by cyclooxygenase-2 (COX-2) and into leukotrienes (LTB 4 ) by 5-lipoxygenase (5-LO). The three inflammatory mediators initiate acute inflammation, including changes in blood flow, increased capillary permeability and inflammatory cell recruitment in the brain injury ambitus zone, including polymorphonuclear leukocytes (i.e., neutrophils) and monocytes. Excess prostaglandins and leukotrienes contribute to chronic inflammation. The neutrophils are activated to further release chemotactic factors, devour necrotic tissue and sterilize bacteria. The influx of monocytes and resident microglial cells develop into macrophages, which secrete pro-inflammatory factors (e.g., TNF-α and IL-1β) and consume foreign bodies, necrotic tissue or apoptotic cells (e.g., efferocytosis). XFZY significantly suppressed the increased levels of blood AA, TNF-α and IL-1β in brain tissue, indicating that XFZY possesses anti-inflammatory effects. To target the PI3K-AKT-mTOR signaling pathway, XFZY significantly reversed the elevated phosphorylation of AKT/mTOR in brain tissue post-TBI, as well as the downstream p70S6K, resulting in a reduced translation ratio of inflammatory factors and exerting anti-inflammatory effects.
Figure Legend Snippet: Inflammatory response in the brain after TBI and the pathomechanism of the anti-inflammatory effect of XFZY. Following TBI, the mechanical injury-stimulated cell membrane releases arachidonic acid (AA), which is metabolized into prostaglandin E2 (PGE2) and prostacyclin (PGI2) by cyclooxygenase-2 (COX-2) and into leukotrienes (LTB 4 ) by 5-lipoxygenase (5-LO). The three inflammatory mediators initiate acute inflammation, including changes in blood flow, increased capillary permeability and inflammatory cell recruitment in the brain injury ambitus zone, including polymorphonuclear leukocytes (i.e., neutrophils) and monocytes. Excess prostaglandins and leukotrienes contribute to chronic inflammation. The neutrophils are activated to further release chemotactic factors, devour necrotic tissue and sterilize bacteria. The influx of monocytes and resident microglial cells develop into macrophages, which secrete pro-inflammatory factors (e.g., TNF-α and IL-1β) and consume foreign bodies, necrotic tissue or apoptotic cells (e.g., efferocytosis). XFZY significantly suppressed the increased levels of blood AA, TNF-α and IL-1β in brain tissue, indicating that XFZY possesses anti-inflammatory effects. To target the PI3K-AKT-mTOR signaling pathway, XFZY significantly reversed the elevated phosphorylation of AKT/mTOR in brain tissue post-TBI, as well as the downstream p70S6K, resulting in a reduced translation ratio of inflammatory factors and exerting anti-inflammatory effects.

Techniques Used: Flow Cytometry, Permeability

Assay of pro-inflammatory cytokine levels in brain tissue. ( A ) The levels of TNF-α in brain lysates from each group. The TNF-α levels were significantly increased in the Vehicle group compared with the Sham group from the 1 st to the 14 th day post-injury, whereas treatment with 9 g/kg XFZY significantly reduced the increase in TNF-α compared with the Vehicle group on the 1 st , 3 rd , 7 th and 14 th days. Treatment with 18 g/kg XFZY significantly reduced the increase in TNF-α levels compared with the Vehicle group on the 1 st , 3 rd and 7 th days (n = 8/group). On the 7 th and 14 th days, the levels of TNF-α in the 9 g/kg XFZY group were significantly lower than those in the 18 g/kg XFZY group. ( B ) The levels of IL-1β in brain lysates in each group. The contents of IL-1β were significantly increased in the Vehicle group compared with the Sham group from the 1 st to the 14 th day post-injury. Treatment with 9 g/kg XFZY significantly reduced the increased levels of IL-1β compared with the Vehicle group on the 1 st , 3 rd , 7 th , and 14 th days. Treatment with 18 g/kg XFZY significantly reduced the increased levels of IL-1β compared with the Vehicle group on the 1 st , 3 rd , 7 th , and 14 th days. On the 3 rd and 7 th days, treatment with 9 g/kg XFZY significantly reduced the levels of IL-1β in the ipsilateral brain tissue compared with treatment with 18 g/kg XFZY (n = 8/group). All of the data were analyzed by two-way ANOVA and are presented as the mean ± SEM. *p
Figure Legend Snippet: Assay of pro-inflammatory cytokine levels in brain tissue. ( A ) The levels of TNF-α in brain lysates from each group. The TNF-α levels were significantly increased in the Vehicle group compared with the Sham group from the 1 st to the 14 th day post-injury, whereas treatment with 9 g/kg XFZY significantly reduced the increase in TNF-α compared with the Vehicle group on the 1 st , 3 rd , 7 th and 14 th days. Treatment with 18 g/kg XFZY significantly reduced the increase in TNF-α levels compared with the Vehicle group on the 1 st , 3 rd and 7 th days (n = 8/group). On the 7 th and 14 th days, the levels of TNF-α in the 9 g/kg XFZY group were significantly lower than those in the 18 g/kg XFZY group. ( B ) The levels of IL-1β in brain lysates in each group. The contents of IL-1β were significantly increased in the Vehicle group compared with the Sham group from the 1 st to the 14 th day post-injury. Treatment with 9 g/kg XFZY significantly reduced the increased levels of IL-1β compared with the Vehicle group on the 1 st , 3 rd , 7 th , and 14 th days. Treatment with 18 g/kg XFZY significantly reduced the increased levels of IL-1β compared with the Vehicle group on the 1 st , 3 rd , 7 th , and 14 th days. On the 3 rd and 7 th days, treatment with 9 g/kg XFZY significantly reduced the levels of IL-1β in the ipsilateral brain tissue compared with treatment with 18 g/kg XFZY (n = 8/group). All of the data were analyzed by two-way ANOVA and are presented as the mean ± SEM. *p

Techniques Used:

2) Product Images from "Changes in ADMA/DDAH Pathway after Hepatic Ischemia/Reperfusion Injury in Rats: The Role of Bile"

Article Title: Changes in ADMA/DDAH Pathway after Hepatic Ischemia/Reperfusion Injury in Rats: The Role of Bile

Journal: BioMed Research International

doi: 10.1155/2014/627434

Hepatic DDAH activity and protein and mRNA expression of DDAH-1 at the end of reperfusion. Livers were submitted to 30 or 60 min ischemia followed by 60 min reperfusion, panel (a). Livers were submitted to 60 min ischemia followed by 60 min reperfusion, panels (b) and (c). Sham-operated control animals had similar manipulation without vascular occlusion. After reperfusion, liver samples were collected from all groups. The results are reported as the mean S.E. of 8 different experiments.
Figure Legend Snippet: Hepatic DDAH activity and protein and mRNA expression of DDAH-1 at the end of reperfusion. Livers were submitted to 30 or 60 min ischemia followed by 60 min reperfusion, panel (a). Livers were submitted to 60 min ischemia followed by 60 min reperfusion, panels (b) and (c). Sham-operated control animals had similar manipulation without vascular occlusion. After reperfusion, liver samples were collected from all groups. The results are reported as the mean S.E. of 8 different experiments.

Techniques Used: Activity Assay, Expressing

3) Product Images from "The role of mononuclear cell tissue factor and inflammatory cytokines in patients with chronic thromboembolic pulmonary hypertension"

Article Title: The role of mononuclear cell tissue factor and inflammatory cytokines in patients with chronic thromboembolic pulmonary hypertension

Journal: Journal of Thrombosis and Thrombolysis

doi: 10.1007/s11239-015-1323-2

Correlation between mPAP and CRP, MCP-1, and TNF-α in CTEPH patients. a Correlation between mPAP and plasma level of CRP. b Correlation between mPAP and plasma level of MCP-1. c Correlation between mPAP and plasma level of TNF-α
Figure Legend Snippet: Correlation between mPAP and CRP, MCP-1, and TNF-α in CTEPH patients. a Correlation between mPAP and plasma level of CRP. b Correlation between mPAP and plasma level of MCP-1. c Correlation between mPAP and plasma level of TNF-α

Techniques Used:

CRP, MCP-1 and TNF-α levels in CTEPH. a Plasma level of CRP in CTEPH (26.44 ± 5.18 mg/L, n = 10), PTE (33.83 ± 21.47 mg/L, n = 20), and non-thromboembolic PH (8.35 ± 5.03 mg/L, n = 15) patients and in control subjects (2.42 ± 1.71 mg/L, n = 20). b Plasma level of MCP-1 in CTEPH (45.49 ± 16.52 pg/mL, n = 10), PTE (69.37 ± 27.58 pg/mL, n = 20), and non-thromboembolic PH (34.20 ± 25.55 pg/mL, n = 15) patients and in control subjects (22.27 ± 8.59 pg/mL, n = 20). c Plasma level of TNF-α in CTEPH (32.34 ± 4.53 pg/mL, n = 10), PTE (31.26 ± 6.62 pg/mL, n = 20), non-thromboembolic PH (23.23 ± 8.44 pg/mL, n = 15) patients and in control subjects (12.12 ± 7.40 pg/mL, n = 20). Plasma concentrations are expressed as mean ± SD. ** P value
Figure Legend Snippet: CRP, MCP-1 and TNF-α levels in CTEPH. a Plasma level of CRP in CTEPH (26.44 ± 5.18 mg/L, n = 10), PTE (33.83 ± 21.47 mg/L, n = 20), and non-thromboembolic PH (8.35 ± 5.03 mg/L, n = 15) patients and in control subjects (2.42 ± 1.71 mg/L, n = 20). b Plasma level of MCP-1 in CTEPH (45.49 ± 16.52 pg/mL, n = 10), PTE (69.37 ± 27.58 pg/mL, n = 20), and non-thromboembolic PH (34.20 ± 25.55 pg/mL, n = 15) patients and in control subjects (22.27 ± 8.59 pg/mL, n = 20). c Plasma level of TNF-α in CTEPH (32.34 ± 4.53 pg/mL, n = 10), PTE (31.26 ± 6.62 pg/mL, n = 20), non-thromboembolic PH (23.23 ± 8.44 pg/mL, n = 15) patients and in control subjects (12.12 ± 7.40 pg/mL, n = 20). Plasma concentrations are expressed as mean ± SD. ** P value

Techniques Used:

Correlation between TF antigen and CRP, MCP-1, and TNF-α levels in patients with CTEPH. a Correlation between TF antigen and plasma level of CRP. b Correlation between TF antigen and plasma level of MCP-1. c Correlation between TF antigen and plasma level of TNF-α
Figure Legend Snippet: Correlation between TF antigen and CRP, MCP-1, and TNF-α levels in patients with CTEPH. a Correlation between TF antigen and plasma level of CRP. b Correlation between TF antigen and plasma level of MCP-1. c Correlation between TF antigen and plasma level of TNF-α

Techniques Used:

4) Product Images from "Calprotectin can play an inflammatory role in acne vulgaris"

Article Title: Calprotectin can play an inflammatory role in acne vulgaris

Journal: Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii

doi: 10.5114/ada.2017.71286

The calprotectin levels of all groups
Figure Legend Snippet: The calprotectin levels of all groups

Techniques Used:

5) Product Images from "Long-term high-fat consumption leads to downregulation of Akt phosphorylation of eNOS at Ser1177 and upregulation of Sirtuin-1 expression in rat cavernous tissue"

Article Title: Long-term high-fat consumption leads to downregulation of Akt phosphorylation of eNOS at Ser1177 and upregulation of Sirtuin-1 expression in rat cavernous tissue

Journal: Age

doi: 10.1007/s11357-013-9591-2

Plasma adiponectin ( a ), soluble vascular cell adhesion protein-1 (sVCAM-1) ( b ), soluble E-selectin ( c ), and oxidized low-density lipoprotein (OxLDL) ( d ) levels in rats from all experimental groups. Values represent the mean value
Figure Legend Snippet: Plasma adiponectin ( a ), soluble vascular cell adhesion protein-1 (sVCAM-1) ( b ), soluble E-selectin ( c ), and oxidized low-density lipoprotein (OxLDL) ( d ) levels in rats from all experimental groups. Values represent the mean value

Techniques Used:

6) Product Images from "Similar and Additive Effects of Ovariectomy and Diabetes on Insulin Resistance and Lipid Metabolism"

Article Title: Similar and Additive Effects of Ovariectomy and Diabetes on Insulin Resistance and Lipid Metabolism

Journal: Biochemistry Research International

doi: 10.1155/2015/567945

Perilipin level (pg/mg protein) in white and brown adipose tissues of different studied groups at the end of the study. The abbreviations denote the following: Sham: sham-operated rats; OVX: ovariectomized rats; WAT: white adipose tissue; BAT: brown adipose tissue. a: significantly different from the sham control group, b: significantly different from the OVX control group, and c: significantly different from the diabetic group, using ANOVA (LSD), P value
Figure Legend Snippet: Perilipin level (pg/mg protein) in white and brown adipose tissues of different studied groups at the end of the study. The abbreviations denote the following: Sham: sham-operated rats; OVX: ovariectomized rats; WAT: white adipose tissue; BAT: brown adipose tissue. a: significantly different from the sham control group, b: significantly different from the OVX control group, and c: significantly different from the diabetic group, using ANOVA (LSD), P value

Techniques Used:

7) Product Images from "Serum AP-endonuclease 1 (sAPE1) as novel biomarker for hepatocellular carcinoma"

Article Title: Serum AP-endonuclease 1 (sAPE1) as novel biomarker for hepatocellular carcinoma

Journal: Oncotarget

doi: 10.18632/oncotarget.26555

sAPE1 level in circulation ( A ) circulating sAPE levels in healthy blood donors, cirrhosis and HCC groups. *** P
Figure Legend Snippet: sAPE1 level in circulation ( A ) circulating sAPE levels in healthy blood donors, cirrhosis and HCC groups. *** P

Techniques Used:

8) Product Images from "Directed self-assembly of herbal small molecules into sustained release hydrogels for treating neural inflammation"

Article Title: Directed self-assembly of herbal small molecules into sustained release hydrogels for treating neural inflammation

Journal: Nature Communications

doi: 10.1038/s41467-019-09601-3

Rhein and rhein hydrogel alleviated neuroinflammation in LPS-induced BV2 cells. a Confocal microscopy images from BV2 cells (treated with control, LPS, rhein and rhein hydrogel). Immunofluorescence staining is shown. Cell nuclei are shown in blue (DAPI), TNF-α is shown in red, IL-1β is shown in green, and yellow labeling represents co-localization. Scale bar, 15 μm. b Representative western blots of TNF-α and IL-1β proteins at 24 h and 48 h. The uncropped and unprocessed scans of blots are presented in Supplementary Fig. 12 . c Quantifications of TNF-α at 24 h and 48 h. d Quantifications of IL-1β proteins at 24 h and 48 h. e – i ELISA assays for determinations of TNF-α ( e ), IL-1β ( f ), IL-6 ( g ), IL-12 ( h ) and iNOS ( i ) levels at 24 h and 48 h. Values are expressed as means ± SEM ( n = 3). One-way ANOVA with Tukey’s post hoc test. * p
Figure Legend Snippet: Rhein and rhein hydrogel alleviated neuroinflammation in LPS-induced BV2 cells. a Confocal microscopy images from BV2 cells (treated with control, LPS, rhein and rhein hydrogel). Immunofluorescence staining is shown. Cell nuclei are shown in blue (DAPI), TNF-α is shown in red, IL-1β is shown in green, and yellow labeling represents co-localization. Scale bar, 15 μm. b Representative western blots of TNF-α and IL-1β proteins at 24 h and 48 h. The uncropped and unprocessed scans of blots are presented in Supplementary Fig. 12 . c Quantifications of TNF-α at 24 h and 48 h. d Quantifications of IL-1β proteins at 24 h and 48 h. e – i ELISA assays for determinations of TNF-α ( e ), IL-1β ( f ), IL-6 ( g ), IL-12 ( h ) and iNOS ( i ) levels at 24 h and 48 h. Values are expressed as means ± SEM ( n = 3). One-way ANOVA with Tukey’s post hoc test. * p

Techniques Used: Confocal Microscopy, Immunofluorescence, Staining, Labeling, Western Blot, Enzyme-linked Immunosorbent Assay

9) Product Images from "Virus-Like Particles Derived From a Virulent Strain of Pest des Petits Ruminants Virus Elicit a More Vigorous Immune Response in Mice and Small Ruminants Than Those From a Vaccine Strain"

Article Title: Virus-Like Particles Derived From a Virulent Strain of Pest des Petits Ruminants Virus Elicit a More Vigorous Immune Response in Mice and Small Ruminants Than Those From a Vaccine Strain

Journal: Frontiers in Microbiology

doi: 10.3389/fmicb.2020.00609

Virus-like particle immunization induces cell-mediated immune response in mice. Splenocytes from mice were stimulated with inactivated PPRV 2 weeks after the third immunization. Splenocytes producing IL-2 (A) , IL-4 (B) , IL-10 (C) , or IFN-γ (D) were identified by ELISpot. Data are depicted as the means ± SD of SFCs per million splenocytes from three mice in each group and were analyzed by one-way ANOVA (* P
Figure Legend Snippet: Virus-like particle immunization induces cell-mediated immune response in mice. Splenocytes from mice were stimulated with inactivated PPRV 2 weeks after the third immunization. Splenocytes producing IL-2 (A) , IL-4 (B) , IL-10 (C) , or IFN-γ (D) were identified by ELISpot. Data are depicted as the means ± SD of SFCs per million splenocytes from three mice in each group and were analyzed by one-way ANOVA (* P

Techniques Used: Mouse Assay, Enzyme-linked Immunospot

Virus-like particle immunization induces significant cytokine response in goats and sheep. (A–D) Serum was collected 3 weeks after the second immunization from animals immunized with PPRV Tibet/30 VLPs, PPRV Nigeria 75/1 VLPs, or adjuvant and were analyzed for the production of IL-2 (A) , IL-4 (B) , IL-10 (C) , and IFN-γ (D) . Data are depicted as the means ± SD for three goats or sheep from each group and were analyzed by one-way ANOVA (* P
Figure Legend Snippet: Virus-like particle immunization induces significant cytokine response in goats and sheep. (A–D) Serum was collected 3 weeks after the second immunization from animals immunized with PPRV Tibet/30 VLPs, PPRV Nigeria 75/1 VLPs, or adjuvant and were analyzed for the production of IL-2 (A) , IL-4 (B) , IL-10 (C) , and IFN-γ (D) . Data are depicted as the means ± SD for three goats or sheep from each group and were analyzed by one-way ANOVA (* P

Techniques Used:

10) Product Images from "Impaired function of the intestinal barrier in a novel sub-health rat model"

Article Title: Impaired function of the intestinal barrier in a novel sub-health rat model

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2016.4978

Production of immune-associated cytokines. (A) Serum level of IFN-γ (pg/ml) in the sub-health group and recovered group were lower than that in the control group, and the levels of IL-4 (pg/ml) in the sub-health group and recovered group were higher than that in the control group. (B) IFN-γ/IL-4 ratios in the sub-health group and recovered group were lower than that in the control group. Data are presented as the mean ± standard deviation. * P
Figure Legend Snippet: Production of immune-associated cytokines. (A) Serum level of IFN-γ (pg/ml) in the sub-health group and recovered group were lower than that in the control group, and the levels of IL-4 (pg/ml) in the sub-health group and recovered group were higher than that in the control group. (B) IFN-γ/IL-4 ratios in the sub-health group and recovered group were lower than that in the control group. Data are presented as the mean ± standard deviation. * P

Techniques Used: Standard Deviation

11) Product Images from "2,3,5,4′-tetrahydroxy-stilbene-2-O-β-D-glucoside attenuates methionine and choline-deficient diet-induced non-alcoholic fatty liver disease"

Article Title: 2,3,5,4′-tetrahydroxy-stilbene-2-O-β-D-glucoside attenuates methionine and choline-deficient diet-induced non-alcoholic fatty liver disease

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2018.6300

Effects of TSG on the protein expression of (A) IL-1β and (B) IL-18 in livers of MCD diet-fed mice. At the end of the experiment, the levels of IL-1β and IL-18 in liver tissue were evaluated. Low dosage of TSG reduced the levels of IL-1β, and high dose of TSG showed that IL-18 levels were reduced compared with the model group. Data are shown as the mean ± SD ( # , compared with the MCD diet-induced NAFLD model group). # P
Figure Legend Snippet: Effects of TSG on the protein expression of (A) IL-1β and (B) IL-18 in livers of MCD diet-fed mice. At the end of the experiment, the levels of IL-1β and IL-18 in liver tissue were evaluated. Low dosage of TSG reduced the levels of IL-1β, and high dose of TSG showed that IL-18 levels were reduced compared with the model group. Data are shown as the mean ± SD ( # , compared with the MCD diet-induced NAFLD model group). # P

Techniques Used: Expressing, Mouse Assay

12) Product Images from "The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction"

Article Title: The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.914916

The effects of remote ischemic conditioning (RIC) on cardiac hemodynamic function and mitochondrial respiratory function in the rat model of acute myocardial infarction (AMI). ( A–D ) The myocardial concentrations of mitochondrial respiratory chain complexes 1, 2, 3, and 4. ( E ) The apoptosis index of the ischemia area for the three groups, the sham group, the AMI group, and the RIC group. ( F ) The serum concentrations of caspase-3 in each of the three rat groups. ( G–I ) The expression of Bcl-2 and Bax protein, and the ratio of Bcl-2/Bax in each group. ( J ) Myocardial cell apoptosis determined by TUNEL staining in rats after AMI. Scale bar=200 μm. (K–L) The levels of ATP and inducible nitric oxide synthase (iNOS) in each group. ( M ) Western blot assay for the protein levels of caspase-3, Bcl-2, and Bax in each group. * P
Figure Legend Snippet: The effects of remote ischemic conditioning (RIC) on cardiac hemodynamic function and mitochondrial respiratory function in the rat model of acute myocardial infarction (AMI). ( A–D ) The myocardial concentrations of mitochondrial respiratory chain complexes 1, 2, 3, and 4. ( E ) The apoptosis index of the ischemia area for the three groups, the sham group, the AMI group, and the RIC group. ( F ) The serum concentrations of caspase-3 in each of the three rat groups. ( G–I ) The expression of Bcl-2 and Bax protein, and the ratio of Bcl-2/Bax in each group. ( J ) Myocardial cell apoptosis determined by TUNEL staining in rats after AMI. Scale bar=200 μm. (K–L) The levels of ATP and inducible nitric oxide synthase (iNOS) in each group. ( M ) Western blot assay for the protein levels of caspase-3, Bcl-2, and Bax in each group. * P

Techniques Used: Expressing, TUNEL Assay, Staining, Western Blot

13) Product Images from "Orphan nuclear receptor SHP regulates iron metabolism through inhibition of BMP6-mediated hepcidin expression"

Article Title: Orphan nuclear receptor SHP regulates iron metabolism through inhibition of BMP6-mediated hepcidin expression

Journal: Scientific Reports

doi: 10.1038/srep34630

Metformin inhibits BMP6-mediated hepcidin gene expression through induction of SHP. ( a ) HepG2 cells were transfected with vectors expressing luciferase under the control of the hepcidin promoter, siControl or siSHP, and treated with BMP6 for 24 h, as indicated. ( b ) HepG2 cells were treated with BMP6, metformin, AICAR or Comp C for 24 h, as indicated in figure. ( c ) Q-PCR analysis showing SHP mRNA levels in AML12 cells infected with Ad-US and Ad-shSHP. ( d ) Q-PCR analysis showing hepcidin (left panel) and SHP (right panel) mRNA levels in AML12 cells. Cells were infected with Ad-US or Ad-shSHP and treated with BMP6 and metformin for 24 h +, 10 MOI. ( e ) Q-PCR analysis showing hepcidin mRNA levels in mouse primary hepatocytes. Cells were infected with Ad-GFP or Ad-AMPK DN and treated with BMP6 and metformin for 24 h +, 10 MOI. ( f ) Q-PCR analysis showing hepcidin mRNA levels in rat primary hepatocytes treated with BMP6 along with metformin, AICAR or compound C for 24 h. ( g ) Hepcidin levels in medium of cultured AML12 cells treated with BMP6 and metformin for 24 h. Data are presented as means ± SD. The experiment was repeated on a minimum of three separate occasions. * P
Figure Legend Snippet: Metformin inhibits BMP6-mediated hepcidin gene expression through induction of SHP. ( a ) HepG2 cells were transfected with vectors expressing luciferase under the control of the hepcidin promoter, siControl or siSHP, and treated with BMP6 for 24 h, as indicated. ( b ) HepG2 cells were treated with BMP6, metformin, AICAR or Comp C for 24 h, as indicated in figure. ( c ) Q-PCR analysis showing SHP mRNA levels in AML12 cells infected with Ad-US and Ad-shSHP. ( d ) Q-PCR analysis showing hepcidin (left panel) and SHP (right panel) mRNA levels in AML12 cells. Cells were infected with Ad-US or Ad-shSHP and treated with BMP6 and metformin for 24 h +, 10 MOI. ( e ) Q-PCR analysis showing hepcidin mRNA levels in mouse primary hepatocytes. Cells were infected with Ad-GFP or Ad-AMPK DN and treated with BMP6 and metformin for 24 h +, 10 MOI. ( f ) Q-PCR analysis showing hepcidin mRNA levels in rat primary hepatocytes treated with BMP6 along with metformin, AICAR or compound C for 24 h. ( g ) Hepcidin levels in medium of cultured AML12 cells treated with BMP6 and metformin for 24 h. Data are presented as means ± SD. The experiment was repeated on a minimum of three separate occasions. * P

Techniques Used: Expressing, Transfection, Luciferase, Polymerase Chain Reaction, Infection, Cell Culture

SHP suppresses BMP6-induced hepcidin gene expression. ( a ) Q-PCR analysis showing hepcidin and SHP mRNA levels in AML12 cells treated with BMP6 (20 nM). ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in mouse hepatocytes treated with BMP6 (20 nM) for 24 h. ( c ) Western blot analysis, showing SHP and AMPK expression in HepG2 cells infected with Ad-GFP, Ad-Flag-SHP and Ad-AMPK ca for 24 h +, 10 MOI. ( d ) Q-PCR analysis showing hepcidin mRNA levels in hepatocytes isolated from wild-type and SHP knockout mice. Hepatocytes were treated with BMP6 (20 nM) and infected with Ad-GFP, Ad-AMPK ca or Ad-Flag-SHP for 24 h. ( e ) Inhibitory effect of SHP on BMP6-mediated induction of mouse and human hepcidin promoter activity. HepG2 cells were transfected with vectors expressing mouse Hepcidin-luc and mSHP or human Hepcidin-luc and hSHP, and treated with BMP6 (20 nM) for 24 h. 2, 200 ng; 4, 400 ng; 6, 600 ng. ( f ) Q-PCR analysis showing hepcidin (left panel) and SHP (right panel) mRNA levels in mouse primary hepatocytes treated with BMP6 or metformin and infected with Ad-GFP, Ad-AMPK ca or Ad-Flag-SHP for 24 h +, 10 MOI. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. Western blot images were cropped with a grey cropping line. All gels for Western blot analysis were run under the same experimental conditions. * P
Figure Legend Snippet: SHP suppresses BMP6-induced hepcidin gene expression. ( a ) Q-PCR analysis showing hepcidin and SHP mRNA levels in AML12 cells treated with BMP6 (20 nM). ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in mouse hepatocytes treated with BMP6 (20 nM) for 24 h. ( c ) Western blot analysis, showing SHP and AMPK expression in HepG2 cells infected with Ad-GFP, Ad-Flag-SHP and Ad-AMPK ca for 24 h +, 10 MOI. ( d ) Q-PCR analysis showing hepcidin mRNA levels in hepatocytes isolated from wild-type and SHP knockout mice. Hepatocytes were treated with BMP6 (20 nM) and infected with Ad-GFP, Ad-AMPK ca or Ad-Flag-SHP for 24 h. ( e ) Inhibitory effect of SHP on BMP6-mediated induction of mouse and human hepcidin promoter activity. HepG2 cells were transfected with vectors expressing mouse Hepcidin-luc and mSHP or human Hepcidin-luc and hSHP, and treated with BMP6 (20 nM) for 24 h. 2, 200 ng; 4, 400 ng; 6, 600 ng. ( f ) Q-PCR analysis showing hepcidin (left panel) and SHP (right panel) mRNA levels in mouse primary hepatocytes treated with BMP6 or metformin and infected with Ad-GFP, Ad-AMPK ca or Ad-Flag-SHP for 24 h +, 10 MOI. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. Western blot images were cropped with a grey cropping line. All gels for Western blot analysis were run under the same experimental conditions. * P

Techniques Used: Expressing, Polymerase Chain Reaction, Western Blot, Infection, Isolation, Knock-Out, Mouse Assay, Activity Assay, Transfection, Molecular Weight

SHP abrogates the BMP6 effect on iron metabolism through inhibition of hepcidin gene expression in mice. ( a – d ) C57/BL6 mice were injected with Ad-GFP ( n = 4 per group, 5.9 × 10 9 pfu) or Ad-Flag-SHP ( n = 5 per group, 5.9 × 10 9 pfu) via the tail-vein, and treated with Vehicle or BMP6 (500 μg/kg, i.p.) for 6 h at day 5 after the infection. ( a ) Serum iron level. ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in liver. ( c ) Serum hepcidin levels. ( d ) Western blot analysis showing SMAD1/5/8 phosphorylation and SHP expression in liver. ( e ) Western blot analysis showing FPN expression in spleen (top). Graphical representation showing FPN expression (bottom). Data are presented as means ± SD. Arrows show locations of molecular weight markers. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. ** P
Figure Legend Snippet: SHP abrogates the BMP6 effect on iron metabolism through inhibition of hepcidin gene expression in mice. ( a – d ) C57/BL6 mice were injected with Ad-GFP ( n = 4 per group, 5.9 × 10 9 pfu) or Ad-Flag-SHP ( n = 5 per group, 5.9 × 10 9 pfu) via the tail-vein, and treated with Vehicle or BMP6 (500 μg/kg, i.p.) for 6 h at day 5 after the infection. ( a ) Serum iron level. ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in liver. ( c ) Serum hepcidin levels. ( d ) Western blot analysis showing SMAD1/5/8 phosphorylation and SHP expression in liver. ( e ) Western blot analysis showing FPN expression in spleen (top). Graphical representation showing FPN expression (bottom). Data are presented as means ± SD. Arrows show locations of molecular weight markers. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. ** P

Techniques Used: Inhibition, Expressing, Mouse Assay, Injection, Infection, Polymerase Chain Reaction, Western Blot, Molecular Weight

SHP represses BMP-mediated SMAD1 transactivation via inhibition of its DNA binding. ( a , b ) HepG2 cells were transfected with BRE-luc reporter plasmid along with vectors expressing SHP or ALK3 CA, and treated with BMP6 or metformin for 24 h. 3, 300 ng; 4, 400 ng; 6, 600 ng. ( c ) HepG2 cells were transfected with vectors expressing luciferase under the control of the hepcidin promoter, Hfe2 or SHP, and treated with metformin for 24 h. 3, 300 ng; 6, 600 ng. ( d ) Western blot analysis showing interaction of SHP and SMADs in 293T cells transfected with vectors expressing myc-SMAD1, myc-SMAD5, myc-SMAD8, HA-SMAD4 and Flag-SHP. The grouping of the image is from different parts of the same gel. ( e ) Q-PCR analysis showing hepcidin mRNA levels (top) and Western blot analysis showing SMAD1 expression (bottom) in mouse primary hepatocytes. Cells were transfected with siCon or siSMAD1 and infected with Ad-GFP or Ad-Flag-SHP. BMP6 was provided for 24 h+, 10 MOI. ( f ) Western blot analysis showing endogenous interaction of SHP and SMAD1 in HepG2 cells treated with BMP6 (20 nM) or metformin (2 mM) for 24 h. ( g ) Western blot analysis (top) and graphical representation (bottom) showing SHP effect on BMP6-medated SMAD1/5/8 phosphorylation. AML12 cells were infected with Ad-GFP or Ad-Flag-SHP (+10 MOI) and treated with BMP6 for 24 h. ( h ) ChIP assay was performed using soluble chromatin immunoprecipitated with anti-SMAD1/5/8, anti-SMAD4, and anti-Flag antibody. Mouse primary hepatocytes were treated with BMP6 for 24 h, and infected with Ad-GFP and Ad-Flag-SHP for 48 h. BMP-RE indicates BMP response element. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P
Figure Legend Snippet: SHP represses BMP-mediated SMAD1 transactivation via inhibition of its DNA binding. ( a , b ) HepG2 cells were transfected with BRE-luc reporter plasmid along with vectors expressing SHP or ALK3 CA, and treated with BMP6 or metformin for 24 h. 3, 300 ng; 4, 400 ng; 6, 600 ng. ( c ) HepG2 cells were transfected with vectors expressing luciferase under the control of the hepcidin promoter, Hfe2 or SHP, and treated with metformin for 24 h. 3, 300 ng; 6, 600 ng. ( d ) Western blot analysis showing interaction of SHP and SMADs in 293T cells transfected with vectors expressing myc-SMAD1, myc-SMAD5, myc-SMAD8, HA-SMAD4 and Flag-SHP. The grouping of the image is from different parts of the same gel. ( e ) Q-PCR analysis showing hepcidin mRNA levels (top) and Western blot analysis showing SMAD1 expression (bottom) in mouse primary hepatocytes. Cells were transfected with siCon or siSMAD1 and infected with Ad-GFP or Ad-Flag-SHP. BMP6 was provided for 24 h+, 10 MOI. ( f ) Western blot analysis showing endogenous interaction of SHP and SMAD1 in HepG2 cells treated with BMP6 (20 nM) or metformin (2 mM) for 24 h. ( g ) Western blot analysis (top) and graphical representation (bottom) showing SHP effect on BMP6-medated SMAD1/5/8 phosphorylation. AML12 cells were infected with Ad-GFP or Ad-Flag-SHP (+10 MOI) and treated with BMP6 for 24 h. ( h ) ChIP assay was performed using soluble chromatin immunoprecipitated with anti-SMAD1/5/8, anti-SMAD4, and anti-Flag antibody. Mouse primary hepatocytes were treated with BMP6 for 24 h, and infected with Ad-GFP and Ad-Flag-SHP for 48 h. BMP-RE indicates BMP response element. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P

Techniques Used: Inhibition, Binding Assay, Transfection, Plasmid Preparation, Expressing, Luciferase, Western Blot, Polymerase Chain Reaction, Infection, Chromatin Immunoprecipitation, Immunoprecipitation, Molecular Weight

Metformin rescues BMP6-mediated alteration of iron metabolism in mice. ( a – e ) C57/BL6 mice ( n = 4 per group) were treated with BMP6 (500 μg/kg, i.p.) and metformin (200 mg/kg, p.o.). ( a ) Serum iron level. ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in liver. ( c ) Serum hepcidin levels. ( d ) Western blot analysis showing SMAD1/5/8 phosphorylation and FPN in liver. ( e ) Western blot analysis (top) and graphical representation (bottom) showing FPN expression in spleen. ( f ) Schematic diagram of SHP-mediated inhibition of BMP6-SMADs pathway. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P
Figure Legend Snippet: Metformin rescues BMP6-mediated alteration of iron metabolism in mice. ( a – e ) C57/BL6 mice ( n = 4 per group) were treated with BMP6 (500 μg/kg, i.p.) and metformin (200 mg/kg, p.o.). ( a ) Serum iron level. ( b ) Q-PCR analysis showing hepcidin and SHP mRNA levels in liver. ( c ) Serum hepcidin levels. ( d ) Western blot analysis showing SMAD1/5/8 phosphorylation and FPN in liver. ( e ) Western blot analysis (top) and graphical representation (bottom) showing FPN expression in spleen. ( f ) Schematic diagram of SHP-mediated inhibition of BMP6-SMADs pathway. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P

Techniques Used: Mouse Assay, Polymerase Chain Reaction, Western Blot, Expressing, Inhibition, Molecular Weight

SHP deficiency alters hepcidin gene expression in liver of HID mice. ( a – i ) WT and SHP KO mice ( n = 5 per group) were fed with high-iron diet (HID, 8 g/kg) for 3 weeks. ( a ) Serum iron level. ( b ) Hepcidin mRNA level in liver. ( c ) Hepcidin expression in mouse liver. IHC was performed using an antibody against hepcidin. Scale bar shows 50 μm. ( d ) Serum hepcidin level. ( e ) Western blot analysis (left panel) showing hepatic SHP and splenic FPN expression and graphical representation (right panel) showing splenic FPN expression. ( f ) Splenic iron level. ( g ) Perls’ prussian blue staining in spleen. Scale bar shows 200 μm. ( h ) BMP6 and BMP9 mRNA levels in liver. ( i ) Western blot analysis (top) and graphical representation (bottom) showing SMAD1/5/8 phosphorylation in liver. The grouping of the images is from different parts of the same gel. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P
Figure Legend Snippet: SHP deficiency alters hepcidin gene expression in liver of HID mice. ( a – i ) WT and SHP KO mice ( n = 5 per group) were fed with high-iron diet (HID, 8 g/kg) for 3 weeks. ( a ) Serum iron level. ( b ) Hepcidin mRNA level in liver. ( c ) Hepcidin expression in mouse liver. IHC was performed using an antibody against hepcidin. Scale bar shows 50 μm. ( d ) Serum hepcidin level. ( e ) Western blot analysis (left panel) showing hepatic SHP and splenic FPN expression and graphical representation (right panel) showing splenic FPN expression. ( f ) Splenic iron level. ( g ) Perls’ prussian blue staining in spleen. Scale bar shows 200 μm. ( h ) BMP6 and BMP9 mRNA levels in liver. ( i ) Western blot analysis (top) and graphical representation (bottom) showing SMAD1/5/8 phosphorylation in liver. The grouping of the images is from different parts of the same gel. Data are presented as means ± SD. Arrows show locations of molecular weight markers. The experiment was repeated on a minimum of three separate occasions. The western blot images were cropped with a grey cropping line. All gels for western blot analysis were run under the same experimental conditions. * P

Techniques Used: Expressing, Mouse Assay, Immunohistochemistry, Western Blot, Staining, Molecular Weight

14) Product Images from "Virus-Like Particles Derived From a Virulent Strain of Pest des Petits Ruminants Virus Elicit a More Vigorous Immune Response in Mice and Small Ruminants Than Those From a Vaccine Strain"

Article Title: Virus-Like Particles Derived From a Virulent Strain of Pest des Petits Ruminants Virus Elicit a More Vigorous Immune Response in Mice and Small Ruminants Than Those From a Vaccine Strain

Journal: Frontiers in Microbiology

doi: 10.3389/fmicb.2020.00609

Virus-like particle immunization induces significant cytokine response in goats and sheep. (A–D) Serum was collected 3 weeks after the second immunization from animals immunized with PPRV Tibet/30 VLPs, PPRV Nigeria 75/1 VLPs, or adjuvant and were analyzed for the production of IL-2 (A) , IL-4 (B) , IL-10 (C) , and IFN-γ (D) . Data are depicted as the means ± SD for three goats or sheep from each group and were analyzed by one-way ANOVA (* P
Figure Legend Snippet: Virus-like particle immunization induces significant cytokine response in goats and sheep. (A–D) Serum was collected 3 weeks after the second immunization from animals immunized with PPRV Tibet/30 VLPs, PPRV Nigeria 75/1 VLPs, or adjuvant and were analyzed for the production of IL-2 (A) , IL-4 (B) , IL-10 (C) , and IFN-γ (D) . Data are depicted as the means ± SD for three goats or sheep from each group and were analyzed by one-way ANOVA (* P

Techniques Used:

15) Product Images from "Prognostic value of Sirtuin1 in acute ischemic stroke and its correlation with functional outcomes"

Article Title: Prognostic value of Sirtuin1 in acute ischemic stroke and its correlation with functional outcomes

Journal: Medicine

doi: 10.1097/MD.0000000000012959

ROC curve of serum SIRT1 activities for diagnosing ischemic stroke patients. ROC = receiver-operating characteristic, SIRT1 = Sirtuin1.
Figure Legend Snippet: ROC curve of serum SIRT1 activities for diagnosing ischemic stroke patients. ROC = receiver-operating characteristic, SIRT1 = Sirtuin1.

Techniques Used:

Linear correlation between serum SIRT1 concentration and NIHSS score. Serum SIRT1 concentration not significantly correlated with NIHSS score ( r = −0.01, P = .920). NIHSS = National Institutes of Health Stroke Scale, SIRT1 = Sirtuin1.
Figure Legend Snippet: Linear correlation between serum SIRT1 concentration and NIHSS score. Serum SIRT1 concentration not significantly correlated with NIHSS score ( r = −0.01, P = .920). NIHSS = National Institutes of Health Stroke Scale, SIRT1 = Sirtuin1.

Techniques Used: Concentration Assay

16) Product Images from "The Evaluation of the Relationship between sTREM-1, VEGF-B, and VEGF Gene Expression Levels with Disease Activity of Behçet's Patients"

Article Title: The Evaluation of the Relationship between sTREM-1, VEGF-B, and VEGF Gene Expression Levels with Disease Activity of Behçet's Patients

Journal: Disease Markers

doi: 10.1155/2018/2649392

The sTREM-1, VEGF-B, and VEGF gene expression levels of Behçet's disease patients and healthy controls.
Figure Legend Snippet: The sTREM-1, VEGF-B, and VEGF gene expression levels of Behçet's disease patients and healthy controls.

Techniques Used: Expressing

17) Product Images from "Calprotectin can play an inflammatory role in acne vulgaris"

Article Title: Calprotectin can play an inflammatory role in acne vulgaris

Journal: Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii

doi: 10.5114/ada.2017.71286

The calprotectin levels of all groups
Figure Legend Snippet: The calprotectin levels of all groups

Techniques Used:

18) Product Images from "Robust Photodynamic Therapy Using 5‐ALA‐Incorporated Nanocomplexes Cures Metastatic Melanoma through Priming of CD4+CD8+ Double Positive T Cells"

Article Title: Robust Photodynamic Therapy Using 5‐ALA‐Incorporated Nanocomplexes Cures Metastatic Melanoma through Priming of CD4+CD8+ Double Positive T Cells

Journal: Advanced Science

doi: 10.1002/advs.201802057

CAH‐mediated PDT highly activated CD4 + CD8 + double positive T cells with elevated proinflammatory cytokines. After two‐circle dosing, fresh excised tumor and spleen from each tested mouse were processed into a single cell suspension, stained with antibodies and analyzed via flow cytometry. A) The percentage of live tumor‐infiltrating T cells marked with CD45 + CD3 + within tumor tissue. B,C) Proportions of CD4 + , CD8 + , CD4 + CD8 + , and other T cells out of total tumor‐infiltrating T cells. D,E) Splenic T cells were marked with CD3, and their subsets were further determined with CD4 and CD8. F) Phenotypes of CD4 + , CD8 + single T cells, and CD4 + CD8 + double positive T cells with indicated surface marker CD44 and CD62L. G) Five CAH (+)‐cured mice were re‐challenged with 10 6 of B16 cells on the opposite flank, and five healthy mice of the same age were used as control. Tumor volume was monitored over time. H) Serum cytokines IL‐2, IL‐6, TNF‐α, and IFN‐γ were measured after two‐circle dosing. Data shown as mean ± S.D. were pooled from at least three independent experiments with at least three mice per group. * p
Figure Legend Snippet: CAH‐mediated PDT highly activated CD4 + CD8 + double positive T cells with elevated proinflammatory cytokines. After two‐circle dosing, fresh excised tumor and spleen from each tested mouse were processed into a single cell suspension, stained with antibodies and analyzed via flow cytometry. A) The percentage of live tumor‐infiltrating T cells marked with CD45 + CD3 + within tumor tissue. B,C) Proportions of CD4 + , CD8 + , CD4 + CD8 + , and other T cells out of total tumor‐infiltrating T cells. D,E) Splenic T cells were marked with CD3, and their subsets were further determined with CD4 and CD8. F) Phenotypes of CD4 + , CD8 + single T cells, and CD4 + CD8 + double positive T cells with indicated surface marker CD44 and CD62L. G) Five CAH (+)‐cured mice were re‐challenged with 10 6 of B16 cells on the opposite flank, and five healthy mice of the same age were used as control. Tumor volume was monitored over time. H) Serum cytokines IL‐2, IL‐6, TNF‐α, and IFN‐γ were measured after two‐circle dosing. Data shown as mean ± S.D. were pooled from at least three independent experiments with at least three mice per group. * p

Techniques Used: Staining, Flow Cytometry, Cytometry, Marker, Mouse Assay

19) Product Images from "2,3,5,4′-tetrahydroxy-stilbene-2-O-β-D-glucoside attenuates methionine and choline-deficient diet-induced non-alcoholic fatty liver disease"

Article Title: 2,3,5,4′-tetrahydroxy-stilbene-2-O-β-D-glucoside attenuates methionine and choline-deficient diet-induced non-alcoholic fatty liver disease

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2018.6300

Effects of TSG on the protein expression of (A) IL-1β and (B) IL-18 in livers of MCD diet-fed mice. At the end of the experiment, the levels of IL-1β and IL-18 in liver tissue were evaluated. Low dosage of TSG reduced the levels of IL-1β, and high dose of TSG showed that IL-18 levels were reduced compared with the model group. Data are shown as the mean ± SD ( # , compared with the MCD diet-induced NAFLD model group). # P
Figure Legend Snippet: Effects of TSG on the protein expression of (A) IL-1β and (B) IL-18 in livers of MCD diet-fed mice. At the end of the experiment, the levels of IL-1β and IL-18 in liver tissue were evaluated. Low dosage of TSG reduced the levels of IL-1β, and high dose of TSG showed that IL-18 levels were reduced compared with the model group. Data are shown as the mean ± SD ( # , compared with the MCD diet-induced NAFLD model group). # P

Techniques Used: Expressing, Mouse Assay

20) Product Images from "Deficiency of Renal Cortical EGF Increases ENaC Activity and Contributes to Salt-Sensitive Hypertension"

Article Title: Deficiency of Renal Cortical EGF Increases ENaC Activity and Contributes to Salt-Sensitive Hypertension

Journal: Journal of the American Society of Nephrology : JASN

doi: 10.1681/ASN.2012080839

EGF concentration in the kidney cortex isolated from SS and SS.13 BN rats fed a LS or HS diet measured with ELISA assay. *** P
Figure Legend Snippet: EGF concentration in the kidney cortex isolated from SS and SS.13 BN rats fed a LS or HS diet measured with ELISA assay. *** P

Techniques Used: Concentration Assay, Isolation, Enzyme-linked Immunosorbent Assay

21) Product Images from "Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord"

Article Title: Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Journal: Cells

doi: 10.3390/cells8111370

Effects of Control-PEBP or PEP-1-PEBP1 on MDA, AOPP, 8-iso-PGF2α, MPO, TNF-α, and HMGB in the spinal cord 72 h after ischemia/reperfusion ( n = 5 per group; a p
Figure Legend Snippet: Effects of Control-PEBP or PEP-1-PEBP1 on MDA, AOPP, 8-iso-PGF2α, MPO, TNF-α, and HMGB in the spinal cord 72 h after ischemia/reperfusion ( n = 5 per group; a p

Techniques Used: Multiple Displacement Amplification

22) Product Images from "Similar and Additive Effects of Ovariectomy and Diabetes on Insulin Resistance and Lipid Metabolism"

Article Title: Similar and Additive Effects of Ovariectomy and Diabetes on Insulin Resistance and Lipid Metabolism

Journal: Biochemistry Research International

doi: 10.1155/2015/567945

Perilipin level (pg/mg protein) in white and brown adipose tissues of different studied groups at the end of the study. The abbreviations denote the following: Sham: sham-operated rats; OVX: ovariectomized rats; WAT: white adipose tissue; BAT: brown adipose tissue. a: significantly different from the sham control group, b: significantly different from the OVX control group, and c: significantly different from the diabetic group, using ANOVA (LSD), P value
Figure Legend Snippet: Perilipin level (pg/mg protein) in white and brown adipose tissues of different studied groups at the end of the study. The abbreviations denote the following: Sham: sham-operated rats; OVX: ovariectomized rats; WAT: white adipose tissue; BAT: brown adipose tissue. a: significantly different from the sham control group, b: significantly different from the OVX control group, and c: significantly different from the diabetic group, using ANOVA (LSD), P value

Techniques Used:

23) Product Images from "The Histone-Deacetylase-Inhibitor Suberoylanilide Hydroxamic Acid Promotes Dental Pulp Repair Mechanisms Through Modulation of Matrix Metalloproteinase-13 Activity"

Article Title: The Histone-Deacetylase-Inhibitor Suberoylanilide Hydroxamic Acid Promotes Dental Pulp Repair Mechanisms Through Modulation of Matrix Metalloproteinase-13 Activity

Journal: Journal of cellular physiology

doi: 10.1002/jcp.25128

The effects of SAHA and MMP-13 activity on dental pulp cell (DPC) migration. (A) Vertical migration of DPCs measured by transwell migration assay at 37°C for 3 h. Positive control (supplemented medium and 10% FCS), 1 and 3μM SAHA had a statistically significantly greater effect on cell migration compared with the negative control. MMP-13i (1 and 2μM) and SAHA in combination with 2μM MMP-13i was not significantly different compared with the negative control, indicating the MMP-13 may be partly responsible for the migratory effects of DPCs. (B) Quantitative data from (C/D) showing cell migration in response to HDACis. (B) Horizontal migration of DPCs by wound healing scratch assay. The effect roles of 1 μm SAHA on the migration and motility of rat DPCs quantified from 24 hour scratch assay. Cells were treated with 1 μM SAHA for 24 h and a scratch made in the confluent cell monolayer. Images were obtained at 0 (Ci–iv) and 24 h post wounding (Di–iv). Values are mean±SEM for 3 independent experiments carried out in triplicate. Asterisks (*) show significant differences compared with control ( P
Figure Legend Snippet: The effects of SAHA and MMP-13 activity on dental pulp cell (DPC) migration. (A) Vertical migration of DPCs measured by transwell migration assay at 37°C for 3 h. Positive control (supplemented medium and 10% FCS), 1 and 3μM SAHA had a statistically significantly greater effect on cell migration compared with the negative control. MMP-13i (1 and 2μM) and SAHA in combination with 2μM MMP-13i was not significantly different compared with the negative control, indicating the MMP-13 may be partly responsible for the migratory effects of DPCs. (B) Quantitative data from (C/D) showing cell migration in response to HDACis. (B) Horizontal migration of DPCs by wound healing scratch assay. The effect roles of 1 μm SAHA on the migration and motility of rat DPCs quantified from 24 hour scratch assay. Cells were treated with 1 μM SAHA for 24 h and a scratch made in the confluent cell monolayer. Images were obtained at 0 (Ci–iv) and 24 h post wounding (Di–iv). Values are mean±SEM for 3 independent experiments carried out in triplicate. Asterisks (*) show significant differences compared with control ( P

Techniques Used: Activity Assay, Migration, Transwell Migration Assay, Positive Control, Negative Control, Wound Healing Assay

The effects of SAHA on MMP-13 protein expression and enzyme activity. (A) Cell lysates from selected time points (1, 7, 14, and 21 days) were normalised using a Bradford dye-binding method and total MMP-13 protein levels quantified for each time point. MMP-13 production was analysed by ELISA. (B) A range of MMP-13i concentrations were added to samples of recombinant MMP-9, −13 and enzyme activity was measured fluorogenically for each inhibitor concentration. MMP-13 activity was blocked dose-dependently, but MMP-9 was not significantly altered. All experimental MMP-13i concentrations tested significantly decreased MMP-13 enzyme activity. (C/D) The effects of SAHA and a pharmacological MMP-13i on MMP-13 enzyme activity in mineralizing DPCs. DPCs were cultured in mineralizing medium±SAHA/MMP-13i and compared with mineralizing and non-mineralizing control cultures at 48 h (C) and 14 days (D). MMP-13 activity (measured fluorogenically) increased in mineralizing culture and in the presence of SAHA at both experimental time-points. As the commercial FRET substrate was preferentially, but not exclusively cleaved by MMP-13, the selective MMP-13 inhibition was used to analyse the role of MMP-13. Selective MMP-13 inhibition significantly reduced enzyme activity in the SAHA cultures. Error bars represent SEM of three independent experiments carried out in triplicate. Significant difference P
Figure Legend Snippet: The effects of SAHA on MMP-13 protein expression and enzyme activity. (A) Cell lysates from selected time points (1, 7, 14, and 21 days) were normalised using a Bradford dye-binding method and total MMP-13 protein levels quantified for each time point. MMP-13 production was analysed by ELISA. (B) A range of MMP-13i concentrations were added to samples of recombinant MMP-9, −13 and enzyme activity was measured fluorogenically for each inhibitor concentration. MMP-13 activity was blocked dose-dependently, but MMP-9 was not significantly altered. All experimental MMP-13i concentrations tested significantly decreased MMP-13 enzyme activity. (C/D) The effects of SAHA and a pharmacological MMP-13i on MMP-13 enzyme activity in mineralizing DPCs. DPCs were cultured in mineralizing medium±SAHA/MMP-13i and compared with mineralizing and non-mineralizing control cultures at 48 h (C) and 14 days (D). MMP-13 activity (measured fluorogenically) increased in mineralizing culture and in the presence of SAHA at both experimental time-points. As the commercial FRET substrate was preferentially, but not exclusively cleaved by MMP-13, the selective MMP-13 inhibition was used to analyse the role of MMP-13. Selective MMP-13 inhibition significantly reduced enzyme activity in the SAHA cultures. Error bars represent SEM of three independent experiments carried out in triplicate. Significant difference P

Techniques Used: Expressing, Activity Assay, Binding Assay, Enzyme-linked Immunosorbent Assay, Recombinant, Concentration Assay, Cell Culture, Inhibition

24) Product Images from "Significant Association Between Low Mitochondrial DNA Content in Peripheral Blood Leukocytes and Ischemic Stroke"

Article Title: Significant Association Between Low Mitochondrial DNA Content in Peripheral Blood Leukocytes and Ischemic Stroke

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

doi: 10.1161/JAHA.117.006157

Correlations of mitochondrial DNA (mt DNA) content with levels of PPARGC 1A and UCP 2 were determined by Spearman rank partial correlation coefficient analyses after adjusting for age, sex, smoking, and alcohol drinking. A, Blue bars show Spearman partial correlation coefficients (ρ) for high mt DNA content (cutoff point ≥1.09) vs peroxisome proliferator‐activated receptor γ coactivator 1α (PPARGC1A) and uncoupling protein 2 (UCP2). B, Red bars show partial correlation coefficients (ρ) for mt DNA content (continuing value) vs PPARGC 1A and UCP 2. A significantly moderate negative correlation was found between mt DNA content and UCP 2. Although PPARGC 1A also negatively correlated with mt DNA content, the result did not reach statistical significance. The asterisk indicates a statistically significant correlation with P
Figure Legend Snippet: Correlations of mitochondrial DNA (mt DNA) content with levels of PPARGC 1A and UCP 2 were determined by Spearman rank partial correlation coefficient analyses after adjusting for age, sex, smoking, and alcohol drinking. A, Blue bars show Spearman partial correlation coefficients (ρ) for high mt DNA content (cutoff point ≥1.09) vs peroxisome proliferator‐activated receptor γ coactivator 1α (PPARGC1A) and uncoupling protein 2 (UCP2). B, Red bars show partial correlation coefficients (ρ) for mt DNA content (continuing value) vs PPARGC 1A and UCP 2. A significantly moderate negative correlation was found between mt DNA content and UCP 2. Although PPARGC 1A also negatively correlated with mt DNA content, the result did not reach statistical significance. The asterisk indicates a statistically significant correlation with P

Techniques Used:

25) Product Images from "Peste des Petits Ruminants Virus-Like Particles Induce a Potent Humoral and Cellular Immune Response in Goats"

Article Title: Peste des Petits Ruminants Virus-Like Particles Induce a Potent Humoral and Cellular Immune Response in Goats

Journal: Viruses

doi: 10.3390/v11100918

Immunization induces a cell-mediated immune response in mice. Splenocytes from mice were stimulated with inactivated PPRV two weeks after the second immunization. ( a ) Representative images of IFN-γ- and IL-4-secreting splenocytes. ( b,c ) ELISpot assay was used to enumerate IFN-γ-secreting (b) or IL-4-secreting (c) splenocytes. Data are depicted as the mean ± SD spot-forming cells (SFCs) per million splenocytes from three mice in each group and were analyzed by one-way ANOVA (* P
Figure Legend Snippet: Immunization induces a cell-mediated immune response in mice. Splenocytes from mice were stimulated with inactivated PPRV two weeks after the second immunization. ( a ) Representative images of IFN-γ- and IL-4-secreting splenocytes. ( b,c ) ELISpot assay was used to enumerate IFN-γ-secreting (b) or IL-4-secreting (c) splenocytes. Data are depicted as the mean ± SD spot-forming cells (SFCs) per million splenocytes from three mice in each group and were analyzed by one-way ANOVA (* P

Techniques Used: Mouse Assay, Enzyme-linked Immunospot

Immunization induces a significant cytokine response in goats. ( a–c ) Serum samples after the second immunization from animals immunized with PPRV VLPs (150 µg or 300 µg), PPRV Nigeria 75/1, PBS, or alum adjuvant were analyzed for IL-4 (a), IL10 (b) and IFN-γ (c). Significant differences were analyzed by one-way ANOVA and indicated as follows: * P
Figure Legend Snippet: Immunization induces a significant cytokine response in goats. ( a–c ) Serum samples after the second immunization from animals immunized with PPRV VLPs (150 µg or 300 µg), PPRV Nigeria 75/1, PBS, or alum adjuvant were analyzed for IL-4 (a), IL10 (b) and IFN-γ (c). Significant differences were analyzed by one-way ANOVA and indicated as follows: * P

Techniques Used:

Immunization improves IFN-γ-secreting CD4+ and CD8+ T cell responses in mice. Two weeks after the second immunization, splenocytes from three mice in each group were cultured and stimulated with inactivated PPRV Nigeria 75/1. Mouse monoclonal antibodies against CD4, CD8, IFN-γ, and IL-4 were used to identify cells that were double-positive ( a ) CD4 + IFN-γ + , ( b ) CD4 + IL-4 + , ( c ) CD8 + IFN-γ + , and ( d ) CD8 + IL-4 + . Data were analyzed by one-way ANOVA and indicated as follows: * P
Figure Legend Snippet: Immunization improves IFN-γ-secreting CD4+ and CD8+ T cell responses in mice. Two weeks after the second immunization, splenocytes from three mice in each group were cultured and stimulated with inactivated PPRV Nigeria 75/1. Mouse monoclonal antibodies against CD4, CD8, IFN-γ, and IL-4 were used to identify cells that were double-positive ( a ) CD4 + IFN-γ + , ( b ) CD4 + IL-4 + , ( c ) CD8 + IFN-γ + , and ( d ) CD8 + IL-4 + . Data were analyzed by one-way ANOVA and indicated as follows: * P

Techniques Used: Mouse Assay, Cell Culture

26) Product Images from "Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH"

Article Title: Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH

Journal: Scientific Reports

doi: 10.1038/srep03822

Tissue levels of TGF-β1 and bFGF in the prostate. Right panel: tissue levels of TGF-β1 in the prostate; Left panel: tissue levels of bFGF in the prostate. WKY: 18-week-old Wistar-Kyoto rat group; SHR: 18-week-old SHR group; Nic3: 18-week-old SHRs treated with nicorandil at a daily dose of 3 mg/kg, i.p.; Nic10: 18-week-old SHRs treated with nicorandil at a daily dose of 10 mg/kg, i.p.; *: Significantly different between groups (P
Figure Legend Snippet: Tissue levels of TGF-β1 and bFGF in the prostate. Right panel: tissue levels of TGF-β1 in the prostate; Left panel: tissue levels of bFGF in the prostate. WKY: 18-week-old Wistar-Kyoto rat group; SHR: 18-week-old SHR group; Nic3: 18-week-old SHRs treated with nicorandil at a daily dose of 3 mg/kg, i.p.; Nic10: 18-week-old SHRs treated with nicorandil at a daily dose of 10 mg/kg, i.p.; *: Significantly different between groups (P

Techniques Used:

27) Product Images from "Impaired function of the intestinal barrier in a novel sub-health rat model"

Article Title: Impaired function of the intestinal barrier in a novel sub-health rat model

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2016.4978

Production of immune-associated cytokines. (A) Serum level of IFN-γ (pg/ml) in the sub-health group and recovered group were lower than that in the control group, and the levels of IL-4 (pg/ml) in the sub-health group and recovered group were higher than that in the control group. (B) IFN-γ/IL-4 ratios in the sub-health group and recovered group were lower than that in the control group. Data are presented as the mean ± standard deviation. * P
Figure Legend Snippet: Production of immune-associated cytokines. (A) Serum level of IFN-γ (pg/ml) in the sub-health group and recovered group were lower than that in the control group, and the levels of IL-4 (pg/ml) in the sub-health group and recovered group were higher than that in the control group. (B) IFN-γ/IL-4 ratios in the sub-health group and recovered group were lower than that in the control group. Data are presented as the mean ± standard deviation. * P

Techniques Used: Standard Deviation

28) Product Images from "Short term resistance training enhanced plasma apoA-I and FABP4 levels in Streptozotocin-induced diabetic rats"

Article Title: Short term resistance training enhanced plasma apoA-I and FABP4 levels in Streptozotocin-induced diabetic rats

Journal: Journal of Diabetes and Metabolic Disorders

doi: 10.1186/2251-6581-13-41

Plasma concentrations of FABP4 in non-diabetic control ( non-DC ), non-diabetic trained ( non-DT ), diabetic control ( DC ), and diabetic trained ( DT ) rats. The values are presented as mean ± standard deviation of 8 animals per group. * P
Figure Legend Snippet: Plasma concentrations of FABP4 in non-diabetic control ( non-DC ), non-diabetic trained ( non-DT ), diabetic control ( DC ), and diabetic trained ( DT ) rats. The values are presented as mean ± standard deviation of 8 animals per group. * P

Techniques Used: Standard Deviation

29) Product Images from "Transcription factor 21 expression in injured podocytes of glomerular diseases"

Article Title: Transcription factor 21 expression in injured podocytes of glomerular diseases

Journal: Scientific Reports

doi: 10.1038/s41598-020-68422-3

In vitro experiments using Tcf21 -expressing murine podocyte cell line. a Based on DEGs of Tcf21-MPs/Control-MPs using microarray, the KEGG pathway frequency analysis presented up-regulated and down-regulated gene groups. b – e : Both cellular morphology of Control-MPs and Tcf21-MPs showed similar shape in low-power ( b , c ) and mid-power magnification ( d , e ). f The area dimension of both MPs was not statistically different (p = 0.54). g In high-power magnification, Tcf21-MP possessed rich actin-stained dendrites, filopodia. h The number of filopodia was significantly higher in Tcf21-MP than in Control-MP (p
Figure Legend Snippet: In vitro experiments using Tcf21 -expressing murine podocyte cell line. a Based on DEGs of Tcf21-MPs/Control-MPs using microarray, the KEGG pathway frequency analysis presented up-regulated and down-regulated gene groups. b – e : Both cellular morphology of Control-MPs and Tcf21-MPs showed similar shape in low-power ( b , c ) and mid-power magnification ( d , e ). f The area dimension of both MPs was not statistically different (p = 0.54). g In high-power magnification, Tcf21-MP possessed rich actin-stained dendrites, filopodia. h The number of filopodia was significantly higher in Tcf21-MP than in Control-MP (p

Techniques Used: In Vitro, Expressing, Microarray, Staining

Anti-apoptotic effect of Tcf21 -expressing murine podocyte cell line using ADR stimulation. a Tcf21-MPs could significantly survive at 48 (p = 0.04) and 72hrs (p
Figure Legend Snippet: Anti-apoptotic effect of Tcf21 -expressing murine podocyte cell line using ADR stimulation. a Tcf21-MPs could significantly survive at 48 (p = 0.04) and 72hrs (p

Techniques Used: Expressing

Histological analysis of TCF21 in human glomerular diseases. a , b The human normal glomeruli showed that TCF21 weakly expressed in the nuclei of podocytes linear marking along with synaptopodin (SYNPO, a ) and nephrin (NPHS1, b ). c In patients with nephrotic syndrome, MGN, NPHS1-stain somewhat decreased, but TCF21 highly expressed in the cellular body of podocytes along the lateral side of NPHS1-positivity. d In the sample of NGD defined score 1, TCF21 weakly expressed in the nuclei of segmental podocytes. e In IgAN sample defined score 2, TCF21 expressed in the nuclei of global podocytes. f In nephrotic syndrome, MGN sample defined score 4, TCF21 expression globally expanded in the cytoplasm of podocytes. g The comparison of TCF21 histological score among various glomerular diseases. Their groups were statistically significant among each glomerular disease (p
Figure Legend Snippet: Histological analysis of TCF21 in human glomerular diseases. a , b The human normal glomeruli showed that TCF21 weakly expressed in the nuclei of podocytes linear marking along with synaptopodin (SYNPO, a ) and nephrin (NPHS1, b ). c In patients with nephrotic syndrome, MGN, NPHS1-stain somewhat decreased, but TCF21 highly expressed in the cellular body of podocytes along the lateral side of NPHS1-positivity. d In the sample of NGD defined score 1, TCF21 weakly expressed in the nuclei of segmental podocytes. e In IgAN sample defined score 2, TCF21 expressed in the nuclei of global podocytes. f In nephrotic syndrome, MGN sample defined score 4, TCF21 expression globally expanded in the cytoplasm of podocytes. g The comparison of TCF21 histological score among various glomerular diseases. Their groups were statistically significant among each glomerular disease (p

Techniques Used: Staining, Expressing

Mechanism hypothesis of TCF21 expression in injured podocytes of glomerular disease. TCF21 expresses in nucleus of normal podocytes on glomerular capillary (left). By contrast, TCF21 highly expresses in both nucleus and cytoplasm of injured podocytes on glomerular disease including nephrotic syndrome (right). Therefore, TCF21 overexpression may have cellular functional effect in injured podocyte. This image was drawn by MEDICAL EDUCATION INC. (Tokyo, Japan), and all copyright was assigned to corresponding author, J.U.
Figure Legend Snippet: Mechanism hypothesis of TCF21 expression in injured podocytes of glomerular disease. TCF21 expresses in nucleus of normal podocytes on glomerular capillary (left). By contrast, TCF21 highly expresses in both nucleus and cytoplasm of injured podocytes on glomerular disease including nephrotic syndrome (right). Therefore, TCF21 overexpression may have cellular functional effect in injured podocyte. This image was drawn by MEDICAL EDUCATION INC. (Tokyo, Japan), and all copyright was assigned to corresponding author, J.U.

Techniques Used: Expressing, Over Expression, Functional Assay

Urinary TCF21 levels in human glomerular diseases. a Urinary TCF21 levels showed a weak positive correlation with urinary protein levels (r 0.4639). b Urinary TCF21 concentration was statistically significant among each glomerular disease, and higher in nephrotic syndrome (p
Figure Legend Snippet: Urinary TCF21 levels in human glomerular diseases. a Urinary TCF21 levels showed a weak positive correlation with urinary protein levels (r 0.4639). b Urinary TCF21 concentration was statistically significant among each glomerular disease, and higher in nephrotic syndrome (p

Techniques Used: Concentration Assay

30) Product Images from "The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction"

Article Title: The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.914916

The effects of remote ischemic conditioning (RIC) on cardiac hemodynamic function and mitochondrial respiratory function in the rat model of acute myocardial infarction (AMI). ( A–D ) The myocardial concentrations of mitochondrial respiratory chain complexes 1, 2, 3, and 4. ( E ) The apoptosis index of the ischemia area for the three groups, the sham group, the AMI group, and the RIC group. ( F ) The serum concentrations of caspase-3 in each of the three rat groups. ( G–I ) The expression of Bcl-2 and Bax protein, and the ratio of Bcl-2/Bax in each group. ( J ) Myocardial cell apoptosis determined by TUNEL staining in rats after AMI. Scale bar=200 μm. (K–L) The levels of ATP and inducible nitric oxide synthase (iNOS) in each group. ( M ) Western blot assay for the protein levels of caspase-3, Bcl-2, and Bax in each group. * P
Figure Legend Snippet: The effects of remote ischemic conditioning (RIC) on cardiac hemodynamic function and mitochondrial respiratory function in the rat model of acute myocardial infarction (AMI). ( A–D ) The myocardial concentrations of mitochondrial respiratory chain complexes 1, 2, 3, and 4. ( E ) The apoptosis index of the ischemia area for the three groups, the sham group, the AMI group, and the RIC group. ( F ) The serum concentrations of caspase-3 in each of the three rat groups. ( G–I ) The expression of Bcl-2 and Bax protein, and the ratio of Bcl-2/Bax in each group. ( J ) Myocardial cell apoptosis determined by TUNEL staining in rats after AMI. Scale bar=200 μm. (K–L) The levels of ATP and inducible nitric oxide synthase (iNOS) in each group. ( M ) Western blot assay for the protein levels of caspase-3, Bcl-2, and Bax in each group. * P

Techniques Used: Expressing, TUNEL Assay, Staining, Western Blot

31) Product Images from "Atheroprotective Effects of Tumor Necrosis Factor–Stimulated Gene-6"

Article Title: Atheroprotective Effects of Tumor Necrosis Factor–Stimulated Gene-6

Journal: JACC: Basic to Translational Science

doi: 10.1016/j.jacbts.2016.07.008

Effects of TSG-6 on ECM Expression in Human VSMCs (A) HASMCs were incubated for 24 h with the indicated concentrations of TSG-6 and were harvested for immunoblotting analyses of collagen-1, collagen-3, TIMP-2, MMP-2, MMP-9, fibronectin, elastin, and α-tubulin. (Top) Representative results of protein expression of each molecule. (Bottom) Densitometric data of each molecule after normalization relative to α-tubulin. n = 4 to 7; *p = 0.025; †p = 0.015; ‡p = 0.047; #p
Figure Legend Snippet: Effects of TSG-6 on ECM Expression in Human VSMCs (A) HASMCs were incubated for 24 h with the indicated concentrations of TSG-6 and were harvested for immunoblotting analyses of collagen-1, collagen-3, TIMP-2, MMP-2, MMP-9, fibronectin, elastin, and α-tubulin. (Top) Representative results of protein expression of each molecule. (Bottom) Densitometric data of each molecule after normalization relative to α-tubulin. n = 4 to 7; *p = 0.025; †p = 0.015; ‡p = 0.047; #p

Techniques Used: Expressing, Incubation

Effects of TSG-6 on Atherosclerotic Lesion Development in ApoE −/− Mice Among 28 ApoE −/− mice at 17 weeks of age, 6 mice were sacrificed before infusion, and 13 and 9 mice were infused with saline (control) or TSG-6 (75 ng/kg/min), respectively, by osmotic minipumps for 4 weeks. The aortic surface was stained by oil red O (A to C) . Cross sections of the aortic sinus were stained with oil red O (D to F) ; antibodies of MOMA-2, a monocyte-macrophage marker (G to I); pentraxin-3, a vascular inflammation marker (J to L) ; α-SMA, a VSMC marker (M to O) ; and Masson’s trichrome, a collagen fiber marker (P to R) . Hematoxylin was used for nuclear staining. (S to X) Comparisons of atherosclerotic lesion area, plaque size, intraplaque monocyte/macrophage and VSMC contents, vascular inflammation, and collagen fibers among the 3 groups. *p
Figure Legend Snippet: Effects of TSG-6 on Atherosclerotic Lesion Development in ApoE −/− Mice Among 28 ApoE −/− mice at 17 weeks of age, 6 mice were sacrificed before infusion, and 13 and 9 mice were infused with saline (control) or TSG-6 (75 ng/kg/min), respectively, by osmotic minipumps for 4 weeks. The aortic surface was stained by oil red O (A to C) . Cross sections of the aortic sinus were stained with oil red O (D to F) ; antibodies of MOMA-2, a monocyte-macrophage marker (G to I); pentraxin-3, a vascular inflammation marker (J to L) ; α-SMA, a VSMC marker (M to O) ; and Masson’s trichrome, a collagen fiber marker (P to R) . Hematoxylin was used for nuclear staining. (S to X) Comparisons of atherosclerotic lesion area, plaque size, intraplaque monocyte/macrophage and VSMC contents, vascular inflammation, and collagen fibers among the 3 groups. *p

Techniques Used: Mouse Assay, Staining, Marker

Effects of TSG-6 on Inflammatory Phenotypes, Cytokine Secretion, Foam Cell Formation, and Related Protein Expression in HMDMs (A) Human monocytes were incubated for the indicated times in RPMI-1640 medium containing 10% human serum with or without TSG-6 (200 ng/ml). Cells were harvested for immunoblotting analysis for CD68 (differentiation marker), MARCO (M1 marker), or MRC1 (M2 marker). β-actin served as a loading control. The graph shows the expressions of MARCO on day 6 and MRC1 on day 3. n = 3; *p
Figure Legend Snippet: Effects of TSG-6 on Inflammatory Phenotypes, Cytokine Secretion, Foam Cell Formation, and Related Protein Expression in HMDMs (A) Human monocytes were incubated for the indicated times in RPMI-1640 medium containing 10% human serum with or without TSG-6 (200 ng/ml). Cells were harvested for immunoblotting analysis for CD68 (differentiation marker), MARCO (M1 marker), or MRC1 (M2 marker). β-actin served as a loading control. The graph shows the expressions of MARCO on day 6 and MRC1 on day 3. n = 3; *p

Techniques Used: Expressing, Incubation, Marker

Expression of TSG-6 in Human Coronary Arteries From Patients Without and With CAD Representative normal coronary arteries (A and B) from a patient with dilated cardiomyopathy (male, age 34 years) and nonstenotic coronary arteries (C and D) from a patient with previous myocardial infarction (male, age 78 years), and representative stenotic coronary arteries (E to I) from a patient with previous myocardial infarction (male, age 62 years) were stained with anti–TSG-6 antibody (A to F) ; anti-α-SMA antibody, a VSMC marker (G) ; Masson’s Trichrome, a collagen fiber marker (H) ; and anti-CD68 antibody, a macrophage marker (I) . These patients died of heart failure or stroke. All coronary arteries were not the culprit artery of acute coronary events. CAD = coronary artery disease; other abbreviations as in Figure 5 .
Figure Legend Snippet: Expression of TSG-6 in Human Coronary Arteries From Patients Without and With CAD Representative normal coronary arteries (A and B) from a patient with dilated cardiomyopathy (male, age 34 years) and nonstenotic coronary arteries (C and D) from a patient with previous myocardial infarction (male, age 78 years), and representative stenotic coronary arteries (E to I) from a patient with previous myocardial infarction (male, age 62 years) were stained with anti–TSG-6 antibody (A to F) ; anti-α-SMA antibody, a VSMC marker (G) ; Masson’s Trichrome, a collagen fiber marker (H) ; and anti-CD68 antibody, a macrophage marker (I) . These patients died of heart failure or stroke. All coronary arteries were not the culprit artery of acute coronary events. CAD = coronary artery disease; other abbreviations as in Figure 5 .

Techniques Used: Expressing, Staining, Marker

Plasma TSG-6 Levels in Patients Without and With CAD Plasma TSG-6 levels were measured by enzyme-linked immunosorbent assay in 47 subjects without CAD and 135 patients with acute coronary syndrome. *p
Figure Legend Snippet: Plasma TSG-6 Levels in Patients Without and With CAD Plasma TSG-6 levels were measured by enzyme-linked immunosorbent assay in 47 subjects without CAD and 135 patients with acute coronary syndrome. *p

Techniques Used: Enzyme-linked Immunosorbent Assay

Effects of TSG-6 on Proliferation, Migration, and Signal Transduction in Human VSMCs (A) Proliferation of HASMCs was determined by WST-8 assay after 48-h incubation in conditioned medium with the indicated concentrations of TSG-6. HASMCs were stained with Giemsa. n = 5; *p = 0.035; †p = 0.029; ‡p
Figure Legend Snippet: Effects of TSG-6 on Proliferation, Migration, and Signal Transduction in Human VSMCs (A) Proliferation of HASMCs was determined by WST-8 assay after 48-h incubation in conditioned medium with the indicated concentrations of TSG-6. HASMCs were stained with Giemsa. n = 5; *p = 0.035; †p = 0.029; ‡p

Techniques Used: Migration, Transduction, Incubation, Staining

Expression of TSG-6 in Human Vascular Cells and its Effects on Inflammatory Response and Proliferation in Human ECs (A) Aliquots of 40 μg of cellular protein from human monocytes, HMDMs, HASMCs, and HUVECs were separated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subjected to immunoblotting analysis for human TSG-6 and β-actin. Immunoblots are representative of 2 independent experiments. (B) Proliferation of EA.hy926 ECs was determined by WST-8 assay after 48-h incubation in DMEM containing 2 concentrations of d -glucose (Glc) (1.0 or 4.5 mg/ml) with the indicated concentrations of TSG-6. EA.hy926 ECs cultured in 4.5 mg/ml d -glucose–conditioned medium were stained by hematoxylin eosin. Glc 1.0 mg/ml (blue) : n = 4; *p
Figure Legend Snippet: Expression of TSG-6 in Human Vascular Cells and its Effects on Inflammatory Response and Proliferation in Human ECs (A) Aliquots of 40 μg of cellular protein from human monocytes, HMDMs, HASMCs, and HUVECs were separated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subjected to immunoblotting analysis for human TSG-6 and β-actin. Immunoblots are representative of 2 independent experiments. (B) Proliferation of EA.hy926 ECs was determined by WST-8 assay after 48-h incubation in DMEM containing 2 concentrations of d -glucose (Glc) (1.0 or 4.5 mg/ml) with the indicated concentrations of TSG-6. EA.hy926 ECs cultured in 4.5 mg/ml d -glucose–conditioned medium were stained by hematoxylin eosin. Glc 1.0 mg/ml (blue) : n = 4; *p

Techniques Used: Expressing, Polyacrylamide Gel Electrophoresis, Western Blot, Incubation, Gas Chromatography, Cell Culture, Staining

Effects of TSG-6 on Inflammatory Phenotype and Marker Expression in Peritoneal Exudate Macrophages From ApoE −/− Mice Peritoneal cells obtained from ApoE −/− mice were suspended in conditioned medium and seeded onto 6-cm dishes (4 × 10 6 cells per 2 ml/dish). After incubation for 1 h at 37°C in 5% CO 2 to allow adhesion, the medium was discarded to remove nonadherent cells. Immediately, adherent macrophages were harvested after washing the dishes with phosphate-buffered saline twice for immunoblotting analyses of MARCO (M1 marker), arginase-1 (M2 marker), MCP-1, pentratin-3, COX-2, NF-κB, JNK, and phosphorylated ERK1/2. β-actin served as a loading control. n = 3 to 5; *p = 0.018; †p = 0.031; ‡p = 0.012; #p = 0.041; §p = 0.038; ¶p
Figure Legend Snippet: Effects of TSG-6 on Inflammatory Phenotype and Marker Expression in Peritoneal Exudate Macrophages From ApoE −/− Mice Peritoneal cells obtained from ApoE −/− mice were suspended in conditioned medium and seeded onto 6-cm dishes (4 × 10 6 cells per 2 ml/dish). After incubation for 1 h at 37°C in 5% CO 2 to allow adhesion, the medium was discarded to remove nonadherent cells. Immediately, adherent macrophages were harvested after washing the dishes with phosphate-buffered saline twice for immunoblotting analyses of MARCO (M1 marker), arginase-1 (M2 marker), MCP-1, pentratin-3, COX-2, NF-κB, JNK, and phosphorylated ERK1/2. β-actin served as a loading control. n = 3 to 5; *p = 0.018; †p = 0.031; ‡p = 0.012; #p = 0.041; §p = 0.038; ¶p

Techniques Used: Marker, Expressing, Mouse Assay, Incubation

32) Product Images from "Relationship between plasma YKL-40 levels and endothelial dysfunction in chronic kidney disease"

Article Title: Relationship between plasma YKL-40 levels and endothelial dysfunction in chronic kidney disease

Journal: Turkish Journal of Medical Sciences

doi: 10.3906/sag-1804-169

Correlation between FMD% and YKL-40 (P
Figure Legend Snippet: Correlation between FMD% and YKL-40 (P

Techniques Used:

Correlation between eGFR and YKL-40 (P
Figure Legend Snippet: Correlation between eGFR and YKL-40 (P

Techniques Used:

Correlation between proteinuria and YKL-40 (P
Figure Legend Snippet: Correlation between proteinuria and YKL-40 (P

Techniques Used:

33) Product Images from "Prostacyclin, thromboxane and glomerular filtration rate are abnormal in sickle cell pregnancy"

Article Title: Prostacyclin, thromboxane and glomerular filtration rate are abnormal in sickle cell pregnancy

Journal: PLoS ONE

doi: 10.1371/journal.pone.0184345

Prostacyclin-to-thromboxane ratio in pregnant and non-pregnant HbSS and HbAA women.
Figure Legend Snippet: Prostacyclin-to-thromboxane ratio in pregnant and non-pregnant HbSS and HbAA women.

Techniques Used:

Relationship between prostacyclin and GFR. A scatter plot showing the relationship between log10 6-keto-PGF1α and estimated creatinine clearance in pregnant HbAA women (N = 20), and HbSS (N = 18) women. The computed best line of fit for both groups of women is displayed and there is a significant positive correlation in HbSS women as shown.
Figure Legend Snippet: Relationship between prostacyclin and GFR. A scatter plot showing the relationship between log10 6-keto-PGF1α and estimated creatinine clearance in pregnant HbAA women (N = 20), and HbSS (N = 18) women. The computed best line of fit for both groups of women is displayed and there is a significant positive correlation in HbSS women as shown.

Techniques Used:

34) Product Images from "Gut ghrelin regulates hepatic glucose production and insulin signaling via a gut-brain-liver pathway"

Article Title: Gut ghrelin regulates hepatic glucose production and insulin signaling via a gut-brain-liver pathway

Journal: Cell Communication and Signaling : CCS

doi: 10.1186/s12964-019-0321-y

Duodenal ghrelin increases hepatic PEPCK, G6Pase and PGC-1α expression through a gut-brain-liver neurocircuitry. Intraduodenal ghrelin infusion in rats increased hepatic PEPCK, G6Pase and PGC-1α mRNA expression ( a ) and PEPCK protein expression ( b ). Rats that received tetracaine ( a and b ), MK-801 in the NTS ( c and d ) or HVAG ( e and f ) failed to respond to duodenal ghrelin to increase hepatic PEPCK, G6Pase and PGC-1α expression. NTS, nucleus of the solitary tract; HVAG, hepatic vagotomy. Values are shown as mean ± SEM. ** P
Figure Legend Snippet: Duodenal ghrelin increases hepatic PEPCK, G6Pase and PGC-1α expression through a gut-brain-liver neurocircuitry. Intraduodenal ghrelin infusion in rats increased hepatic PEPCK, G6Pase and PGC-1α mRNA expression ( a ) and PEPCK protein expression ( b ). Rats that received tetracaine ( a and b ), MK-801 in the NTS ( c and d ) or HVAG ( e and f ) failed to respond to duodenal ghrelin to increase hepatic PEPCK, G6Pase and PGC-1α expression. NTS, nucleus of the solitary tract; HVAG, hepatic vagotomy. Values are shown as mean ± SEM. ** P

Techniques Used: Pyrolysis Gas Chromatography, Expressing

Gut ghrelin attenuated hepatic insulin signaling through a gut-brain- liver neurocircuitry. Intraduodenal ghrelin infusion decreased the phosphorylation of InsR ( a ) and AKT ( b ) in the liver of rats. Rats that received tetracaine ( a and b ), MK-801 in the NTS ( c and d ) or HVAG ( e and f ) failed to respond to duodenal ghrelin to decrease the phosphorylation of InsR (Tyr 1150/1151) and AKT (Ser473) in the liver of rats. InsR, insulin receptor; AKT, protein kinase B; NTS, nucleus of the solitary tract; HVAG, hepatic vagotomy. Values are shown as mean ± SEM. ** P
Figure Legend Snippet: Gut ghrelin attenuated hepatic insulin signaling through a gut-brain- liver neurocircuitry. Intraduodenal ghrelin infusion decreased the phosphorylation of InsR ( a ) and AKT ( b ) in the liver of rats. Rats that received tetracaine ( a and b ), MK-801 in the NTS ( c and d ) or HVAG ( e and f ) failed to respond to duodenal ghrelin to decrease the phosphorylation of InsR (Tyr 1150/1151) and AKT (Ser473) in the liver of rats. InsR, insulin receptor; AKT, protein kinase B; NTS, nucleus of the solitary tract; HVAG, hepatic vagotomy. Values are shown as mean ± SEM. ** P

Techniques Used:

A schematic model showing the effects of duodenal ghrelin on hepatic glucose fluxes and insulin signals. Ghrelin binds to its receptor, GHS-R1a, on the duodenum and inhibits mucosal AMPK. This signal is delivered to the NTS by vagus afferent nerve and activates the neurons in hindbrain region and NMDA receptors. Finally, the signal is relayed from the NTS to the liver via the efferent branch of the vagal nerve to increase HGP and inhibit insulin signal
Figure Legend Snippet: A schematic model showing the effects of duodenal ghrelin on hepatic glucose fluxes and insulin signals. Ghrelin binds to its receptor, GHS-R1a, on the duodenum and inhibits mucosal AMPK. This signal is delivered to the NTS by vagus afferent nerve and activates the neurons in hindbrain region and NMDA receptors. Finally, the signal is relayed from the NTS to the liver via the efferent branch of the vagal nerve to increase HGP and inhibit insulin signal

Techniques Used:

Gut ghrelin increases liver glucose production through ghrelin-receptor (GHS-R1a). a Photomicrographs of GHS-R1a immunostaining incubated with saline or GHS-R1a antibody in rat duodenal tissues. Arrowheads indicate positive cells for GHS-R1a staining. b Immunofluorescent images of duodenal tissue sections stained for GHS-R1a (green) and ghrelin (red). c Schematic representation of working hypothesis. Ghrelin with or without GHS-R1a antagonist ([D-Lys 3 ]-GHRP-6) was infused through a duodenal catheter. d Experimental procedure and clamp protocol. Duodenal catheter or venous and arterial catheters were implanted on day 1. The pancreatic clamp studies were performed on day 5. e Gut ghrelin decreased GIR in dose dependent manner. f Cumulative GIR during the steady-state of clamp. g HGP. h Suppression of HGP during the clamp period expressed as the percentage reduction from basal HGP. i Glucose uptake. GIR, the rate of glucose infusion; HGP, hepatic glucose production. Data are means ± SEM, ** P
Figure Legend Snippet: Gut ghrelin increases liver glucose production through ghrelin-receptor (GHS-R1a). a Photomicrographs of GHS-R1a immunostaining incubated with saline or GHS-R1a antibody in rat duodenal tissues. Arrowheads indicate positive cells for GHS-R1a staining. b Immunofluorescent images of duodenal tissue sections stained for GHS-R1a (green) and ghrelin (red). c Schematic representation of working hypothesis. Ghrelin with or without GHS-R1a antagonist ([D-Lys 3 ]-GHRP-6) was infused through a duodenal catheter. d Experimental procedure and clamp protocol. Duodenal catheter or venous and arterial catheters were implanted on day 1. The pancreatic clamp studies were performed on day 5. e Gut ghrelin decreased GIR in dose dependent manner. f Cumulative GIR during the steady-state of clamp. g HGP. h Suppression of HGP during the clamp period expressed as the percentage reduction from basal HGP. i Glucose uptake. GIR, the rate of glucose infusion; HGP, hepatic glucose production. Data are means ± SEM, ** P

Techniques Used: Immunostaining, Incubation, Staining

Gut ghrelin increases hepatic glucose production by activating a gut-brain-liver neurocircuitry. a Schematic representation of the working hypothesis. Gut ghrelin was coinfused with tetracaine, which abolishes the ascending neuronal signal to the brain. A subgroup of rats was given MK-801, an NMDA receptor inhibitor, directly into the NTS. In another study, gut ghrelin was infused into rats with HVAG. b Experimental procedure and clamp protocol. Stereotaxic surgeries were conducted on day 1. A duodenal catheter or venous and arterial catheters were implanted on day 7. HVAG was performed immediately before the implantation of the duodenal and vascular catheters. c and d Gut ghrelin infusion decreased GIR and increased HGP. Rats that received tetracaine in the gut, MK-801 in the NTS or HVAG failed to respond to duodenal ghrelin to decrease the GIR and increase HGP. e Suppression of HGP during the clamp expressed as the percentage decrease from basal HGP. f Glucose uptake was unchanged in all groups. NTS, the nucleus of the solitary tract; HVAG, hepatic vagotomy; NMDA, N -methyl- D-aspartate; GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P
Figure Legend Snippet: Gut ghrelin increases hepatic glucose production by activating a gut-brain-liver neurocircuitry. a Schematic representation of the working hypothesis. Gut ghrelin was coinfused with tetracaine, which abolishes the ascending neuronal signal to the brain. A subgroup of rats was given MK-801, an NMDA receptor inhibitor, directly into the NTS. In another study, gut ghrelin was infused into rats with HVAG. b Experimental procedure and clamp protocol. Stereotaxic surgeries were conducted on day 1. A duodenal catheter or venous and arterial catheters were implanted on day 7. HVAG was performed immediately before the implantation of the duodenal and vascular catheters. c and d Gut ghrelin infusion decreased GIR and increased HGP. Rats that received tetracaine in the gut, MK-801 in the NTS or HVAG failed to respond to duodenal ghrelin to decrease the GIR and increase HGP. e Suppression of HGP during the clamp expressed as the percentage decrease from basal HGP. f Glucose uptake was unchanged in all groups. NTS, the nucleus of the solitary tract; HVAG, hepatic vagotomy; NMDA, N -methyl- D-aspartate; GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P

Techniques Used:

Gut ghrelin increases HGP through AMPK inhibition. a Schematic of the working hypothesis. b Experimental procedure and clamp protocol. Ghrelin was infused with or without AICAR, an AMPK activator, through a duodenal catheter. c Representative western blots of AMPK in the mucosal layer of the duodenum. d Gut ghrelin infusion decreased the GIR. When duodenal ghrelin was co-infused with AICAR, the effects of ghrelin on GIR were abolished. GIR, glucose infusion rate. Values are shown as mean ± SEM. * P
Figure Legend Snippet: Gut ghrelin increases HGP through AMPK inhibition. a Schematic of the working hypothesis. b Experimental procedure and clamp protocol. Ghrelin was infused with or without AICAR, an AMPK activator, through a duodenal catheter. c Representative western blots of AMPK in the mucosal layer of the duodenum. d Gut ghrelin infusion decreased the GIR. When duodenal ghrelin was co-infused with AICAR, the effects of ghrelin on GIR were abolished. GIR, glucose infusion rate. Values are shown as mean ± SEM. * P

Techniques Used: Inhibition, Western Blot

Gut ghrelin infusion disrupts the gut nutrient sensing-related mechanisms. a Schematic representation of the working hypothesis. Lipid with or without ghrelin, or saline was infused through a duodenal catheter. b Experimental procedure and clamp protocol. c-e Gut lipids infusion increased the GIR ( c ), and decreased HGP ( d and e ). When duodenal lipid was co-infused with ghrelin, the effects of lipids on GIR and HGP were abolished. f Glucose uptake was unchanged in all groups. g - i The effect of gut ghrelin on glucose homeostasis during fasting-refeeding. g Schematic representation of the experimental design. A duodenal catheter, the internal jugular vein and carotid artery catheters were implanted on day 1. Rats were subjected to a 40 h fasting from 5 p.m. on day 5 until 9 a.m. on day 7. Ten minutes before the completion of the forty-hour fast, rats were infused with intraduodenal saline or ghrelin (n = 5 per group). Rats were refed on regular chow at time 0 min where food intake and blood glucose were monitored for 20 min. h Plasma glucose levels during refeeding. i Cumulative food intake during refeeding. GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P
Figure Legend Snippet: Gut ghrelin infusion disrupts the gut nutrient sensing-related mechanisms. a Schematic representation of the working hypothesis. Lipid with or without ghrelin, or saline was infused through a duodenal catheter. b Experimental procedure and clamp protocol. c-e Gut lipids infusion increased the GIR ( c ), and decreased HGP ( d and e ). When duodenal lipid was co-infused with ghrelin, the effects of lipids on GIR and HGP were abolished. f Glucose uptake was unchanged in all groups. g - i The effect of gut ghrelin on glucose homeostasis during fasting-refeeding. g Schematic representation of the experimental design. A duodenal catheter, the internal jugular vein and carotid artery catheters were implanted on day 1. Rats were subjected to a 40 h fasting from 5 p.m. on day 5 until 9 a.m. on day 7. Ten minutes before the completion of the forty-hour fast, rats were infused with intraduodenal saline or ghrelin (n = 5 per group). Rats were refed on regular chow at time 0 min where food intake and blood glucose were monitored for 20 min. h Plasma glucose levels during refeeding. i Cumulative food intake during refeeding. GIR, glucose infusion rate; HGP, hepatic glucose production. Values are shown as mean ± SEM. * P

Techniques Used:

35) Product Images from "Strontium Chloride: Can It Be a New Treatment Option for Ulcerative Colitis?"

Article Title: Strontium Chloride: Can It Be a New Treatment Option for Ulcerative Colitis?

Journal: BioMed Research International

doi: 10.1155/2014/530687

Comparison of neopterin levels among groups. The horizontal lines in the middle of each box indicate the median, while the top and bottom borders of the box mark the 25th and 75th percentiles, respectively. The whiskers above and below the box mark the maximum and minimum neopterin levels. Open circles indicate outliers. Asterisks represent extreme cases.
Figure Legend Snippet: Comparison of neopterin levels among groups. The horizontal lines in the middle of each box indicate the median, while the top and bottom borders of the box mark the 25th and 75th percentiles, respectively. The whiskers above and below the box mark the maximum and minimum neopterin levels. Open circles indicate outliers. Asterisks represent extreme cases.

Techniques Used:

36) Product Images from "Prognostic value of Sirtuin1 in acute ischemic stroke and its correlation with functional outcomes"

Article Title: Prognostic value of Sirtuin1 in acute ischemic stroke and its correlation with functional outcomes

Journal: Medicine

doi: 10.1097/MD.0000000000012959

ROC curve of serum SIRT1 activities for diagnosing ischemic stroke patients. ROC = receiver-operating characteristic, SIRT1 = Sirtuin1.
Figure Legend Snippet: ROC curve of serum SIRT1 activities for diagnosing ischemic stroke patients. ROC = receiver-operating characteristic, SIRT1 = Sirtuin1.

Techniques Used:

Linear correlation between serum SIRT1 concentration and NIHSS score. Serum SIRT1 concentration not significantly correlated with NIHSS score ( r = −0.01, P = .920). NIHSS = National Institutes of Health Stroke Scale, SIRT1 = Sirtuin1.
Figure Legend Snippet: Linear correlation between serum SIRT1 concentration and NIHSS score. Serum SIRT1 concentration not significantly correlated with NIHSS score ( r = −0.01, P = .920). NIHSS = National Institutes of Health Stroke Scale, SIRT1 = Sirtuin1.

Techniques Used: Concentration Assay

37) Product Images from "The Histone-Deacetylase-Inhibitor Suberoylanilide Hydroxamic Acid Promotes Dental Pulp Repair Mechanisms Through Modulation of Matrix Metalloproteinase-13 Activity"

Article Title: The Histone-Deacetylase-Inhibitor Suberoylanilide Hydroxamic Acid Promotes Dental Pulp Repair Mechanisms Through Modulation of Matrix Metalloproteinase-13 Activity

Journal: Journal of cellular physiology

doi: 10.1002/jcp.25128

The effects of SAHA on MMP-13 protein expression and enzyme activity. (A) Cell lysates from selected time points (1, 7, 14, and 21 days) were normalised using a Bradford dye-binding method and total MMP-13 protein levels quantified for each time point. MMP-13 production was analysed by ELISA. (B) A range of MMP-13i concentrations were added to samples of recombinant MMP-9, −13 and enzyme activity was measured fluorogenically for each inhibitor concentration. MMP-13 activity was blocked dose-dependently, but MMP-9 was not significantly altered. All experimental MMP-13i concentrations tested significantly decreased MMP-13 enzyme activity. (C/D) The effects of SAHA and a pharmacological MMP-13i on MMP-13 enzyme activity in mineralizing DPCs. DPCs were cultured in mineralizing medium±SAHA/MMP-13i and compared with mineralizing and non-mineralizing control cultures at 48 h (C) and 14 days (D). MMP-13 activity (measured fluorogenically) increased in mineralizing culture and in the presence of SAHA at both experimental time-points. As the commercial FRET substrate was preferentially, but not exclusively cleaved by MMP-13, the selective MMP-13 inhibition was used to analyse the role of MMP-13. Selective MMP-13 inhibition significantly reduced enzyme activity in the SAHA cultures. Error bars represent SEM of three independent experiments carried out in triplicate. Significant difference P
Figure Legend Snippet: The effects of SAHA on MMP-13 protein expression and enzyme activity. (A) Cell lysates from selected time points (1, 7, 14, and 21 days) were normalised using a Bradford dye-binding method and total MMP-13 protein levels quantified for each time point. MMP-13 production was analysed by ELISA. (B) A range of MMP-13i concentrations were added to samples of recombinant MMP-9, −13 and enzyme activity was measured fluorogenically for each inhibitor concentration. MMP-13 activity was blocked dose-dependently, but MMP-9 was not significantly altered. All experimental MMP-13i concentrations tested significantly decreased MMP-13 enzyme activity. (C/D) The effects of SAHA and a pharmacological MMP-13i on MMP-13 enzyme activity in mineralizing DPCs. DPCs were cultured in mineralizing medium±SAHA/MMP-13i and compared with mineralizing and non-mineralizing control cultures at 48 h (C) and 14 days (D). MMP-13 activity (measured fluorogenically) increased in mineralizing culture and in the presence of SAHA at both experimental time-points. As the commercial FRET substrate was preferentially, but not exclusively cleaved by MMP-13, the selective MMP-13 inhibition was used to analyse the role of MMP-13. Selective MMP-13 inhibition significantly reduced enzyme activity in the SAHA cultures. Error bars represent SEM of three independent experiments carried out in triplicate. Significant difference P

Techniques Used: Expressing, Activity Assay, Binding Assay, Enzyme-linked Immunosorbent Assay, Recombinant, Concentration Assay, Cell Culture, Inhibition

38) Product Images from "Transcription factor 21 expression in injured podocytes of glomerular diseases"

Article Title: Transcription factor 21 expression in injured podocytes of glomerular diseases

Journal: Scientific Reports

doi: 10.1038/s41598-020-68422-3

In vitro experiments using Tcf21 -expressing murine podocyte cell line. a Based on DEGs of Tcf21-MPs/Control-MPs using microarray, the KEGG pathway frequency analysis presented up-regulated and down-regulated gene groups. b – e : Both cellular morphology of Control-MPs and Tcf21-MPs showed similar shape in low-power ( b , c ) and mid-power magnification ( d , e ). f The area dimension of both MPs was not statistically different (p = 0.54). g In high-power magnification, Tcf21-MP possessed rich actin-stained dendrites, filopodia. h The number of filopodia was significantly higher in Tcf21-MP than in Control-MP (p
Figure Legend Snippet: In vitro experiments using Tcf21 -expressing murine podocyte cell line. a Based on DEGs of Tcf21-MPs/Control-MPs using microarray, the KEGG pathway frequency analysis presented up-regulated and down-regulated gene groups. b – e : Both cellular morphology of Control-MPs and Tcf21-MPs showed similar shape in low-power ( b , c ) and mid-power magnification ( d , e ). f The area dimension of both MPs was not statistically different (p = 0.54). g In high-power magnification, Tcf21-MP possessed rich actin-stained dendrites, filopodia. h The number of filopodia was significantly higher in Tcf21-MP than in Control-MP (p

Techniques Used: In Vitro, Expressing, Microarray, Staining

Anti-apoptotic effect of Tcf21 -expressing murine podocyte cell line using ADR stimulation. a Tcf21-MPs could significantly survive at 48 (p = 0.04) and 72hrs (p
Figure Legend Snippet: Anti-apoptotic effect of Tcf21 -expressing murine podocyte cell line using ADR stimulation. a Tcf21-MPs could significantly survive at 48 (p = 0.04) and 72hrs (p

Techniques Used: Expressing

Histological analysis of TCF21 in human glomerular diseases. a , b The human normal glomeruli showed that TCF21 weakly expressed in the nuclei of podocytes linear marking along with synaptopodin (SYNPO, a ) and nephrin (NPHS1, b ). c In patients with nephrotic syndrome, MGN, NPHS1-stain somewhat decreased, but TCF21 highly expressed in the cellular body of podocytes along the lateral side of NPHS1-positivity. d In the sample of NGD defined score 1, TCF21 weakly expressed in the nuclei of segmental podocytes. e In IgAN sample defined score 2, TCF21 expressed in the nuclei of global podocytes. f In nephrotic syndrome, MGN sample defined score 4, TCF21 expression globally expanded in the cytoplasm of podocytes. g The comparison of TCF21 histological score among various glomerular diseases. Their groups were statistically significant among each glomerular disease (p
Figure Legend Snippet: Histological analysis of TCF21 in human glomerular diseases. a , b The human normal glomeruli showed that TCF21 weakly expressed in the nuclei of podocytes linear marking along with synaptopodin (SYNPO, a ) and nephrin (NPHS1, b ). c In patients with nephrotic syndrome, MGN, NPHS1-stain somewhat decreased, but TCF21 highly expressed in the cellular body of podocytes along the lateral side of NPHS1-positivity. d In the sample of NGD defined score 1, TCF21 weakly expressed in the nuclei of segmental podocytes. e In IgAN sample defined score 2, TCF21 expressed in the nuclei of global podocytes. f In nephrotic syndrome, MGN sample defined score 4, TCF21 expression globally expanded in the cytoplasm of podocytes. g The comparison of TCF21 histological score among various glomerular diseases. Their groups were statistically significant among each glomerular disease (p

Techniques Used: Staining, Expressing

Mechanism hypothesis of TCF21 expression in injured podocytes of glomerular disease. TCF21 expresses in nucleus of normal podocytes on glomerular capillary (left). By contrast, TCF21 highly expresses in both nucleus and cytoplasm of injured podocytes on glomerular disease including nephrotic syndrome (right). Therefore, TCF21 overexpression may have cellular functional effect in injured podocyte. This image was drawn by MEDICAL EDUCATION INC. (Tokyo, Japan), and all copyright was assigned to corresponding author, J.U.
Figure Legend Snippet: Mechanism hypothesis of TCF21 expression in injured podocytes of glomerular disease. TCF21 expresses in nucleus of normal podocytes on glomerular capillary (left). By contrast, TCF21 highly expresses in both nucleus and cytoplasm of injured podocytes on glomerular disease including nephrotic syndrome (right). Therefore, TCF21 overexpression may have cellular functional effect in injured podocyte. This image was drawn by MEDICAL EDUCATION INC. (Tokyo, Japan), and all copyright was assigned to corresponding author, J.U.

Techniques Used: Expressing, Over Expression, Functional Assay

Urinary TCF21 levels in human glomerular diseases. a Urinary TCF21 levels showed a weak positive correlation with urinary protein levels (r 0.4639). b Urinary TCF21 concentration was statistically significant among each glomerular disease, and higher in nephrotic syndrome (p
Figure Legend Snippet: Urinary TCF21 levels in human glomerular diseases. a Urinary TCF21 levels showed a weak positive correlation with urinary protein levels (r 0.4639). b Urinary TCF21 concentration was statistically significant among each glomerular disease, and higher in nephrotic syndrome (p

Techniques Used: Concentration Assay

39) Product Images from "Serum 8-OHdG and HIF-1? levels: do they affect the development of malignancy in patients with hypoactive thyroid nodules?"

Article Title: Serum 8-OHdG and HIF-1? levels: do they affect the development of malignancy in patients with hypoactive thyroid nodules?

Journal: Contemporary Oncology

doi: 10.5114/wo.2013.33774

Examination of HIF-1α cytokine between the patient and the control groups. A difference is determined between the patients and the control group in terms of HIF-1α levels ( p
Figure Legend Snippet: Examination of HIF-1α cytokine between the patient and the control groups. A difference is determined between the patients and the control group in terms of HIF-1α levels ( p

Techniques Used:

40) Product Images from "Controlled-release levodopa methyl ester/benserazide-loaded nanoparticles ameliorate levodopa-induced dyskinesia in rats"

Article Title: Controlled-release levodopa methyl ester/benserazide-loaded nanoparticles ameliorate levodopa-induced dyskinesia in rats

Journal: International Journal of Nanomedicine

doi: 10.2147/IJN.S30463

Effect of administration of LDME/benserazide-loaded nanoparticles on dynorphin levels in the striatum ( A ) and cortex ( B ) of dyskinetic rats. The levels of dynorphin were evaluated by ELISA. The results showed that after repeated administration of LDME plus benserazide, dynorphin increased significantly in dyskinetic rats. However, administration of LDME/benserazide-loaded nanoparticles decreased dynorphin levels in dyskinetic rats. Notes: ( A ) * P
Figure Legend Snippet: Effect of administration of LDME/benserazide-loaded nanoparticles on dynorphin levels in the striatum ( A ) and cortex ( B ) of dyskinetic rats. The levels of dynorphin were evaluated by ELISA. The results showed that after repeated administration of LDME plus benserazide, dynorphin increased significantly in dyskinetic rats. However, administration of LDME/benserazide-loaded nanoparticles decreased dynorphin levels in dyskinetic rats. Notes: ( A ) * P

Techniques Used: Enzyme-linked Immunosorbent Assay

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Article Snippet: .. BCL-2 and caspase-9 levels were measured in liver tissue homogenate by ELISA using kits supplied by CUSABIO and CusAb (Wuhan, China). .. Determination of MMP-2 and TIMP-1 levels Following the manufacturer’s protocol, MMP-2 and TIMP-1 levels were estimated in liver tissue homogenate using ELISA kits obtained from R & D Systems.

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Article Snippet: .. An enzyme-linked immunoassay (ELISA) method was used with primary antibodies to Bcl-2, and Bax (Cusabio, Houston, TX, USA) and to caspase-3 (LifeSpan BioScience, Seattle, WA, USA), according to the manufacturer’s instructions. .. Measurement of apoptosis in the rat myocardium Apoptosis was examined using the TUNEL with an Apoptosis Detection Kit (Roche, Basel, Switzerland), according to the manufacturer’s instructions.

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