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tbms1  (MedChemExpress)


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    Structured Review

    MedChemExpress tbms1
    Tbms1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n0890/Tubeimoside+I/10__37290_slash_ctnr2641___452x__22_ascii58_861___867-43-0-2
    Average 94 stars, based on 5 article reviews
    tbms1 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

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    Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation.
    Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

    Article Title: Targeted ferroptosis of myofibroblasts by tubeimoside I attenuates hypertrophic scar formation
    Article Snippet: TBMS1 (MCE, HY-N0890), ferrostatin-1 (MCE, HY-100579), necrosulfonamide (MCE, HY-100573), 740Y-P (MCE, HY-P0175), Z-VAD-FMK (MCE, HY-16658B), Erastin (MCE, HY-15763) and ML385 (MCE, HY-100523) were used.

    High Performance Liquid Chromatography:

    Article Title: Engineered MAP30ER: A plant toxin-derived platform for EGFR-Targeted delivery of protein and chemotherapeutic payloads.
    Article Snippet: The nonspecific toxicity of traditional chemotherapeutic agents and the intracellular delivery barriers of proteinbased drugs have limited their clinical applications.. Efficient targeted delivery properties of toxin proteins themselves provide important insights into the design of novel drug delivery systems.. Inspired by the natural targeting properties of the plant-derived type I ribosome-inactivating protein (RIPs) MAP30, we engineered a detoxified carrier, MAP30ER, through site-directed mutagenesis of key enzymatic residues (E158A/R161A).

    CCK-8 Assay:

    Article Title: Tubeimoside Ⅰ Targets Sodium/Potassium ATPase alpha 1 Subunit to Selectively Eliminate Senescent Cells and Alleviate Aging-associated Abnormalities
    Article Snippet: Background: Senescent cells accumulate with age and contribute to age-related diseases, which makes their selective elimination a promising strategy for therapeutic intervention.. Tubeimoside I (TBMS1), a natural triterpenoid saponin derived from Bolbostemma paniculatum, has been extensively studied for its anticancer properties.. However, its potential role as a senolytics has yet to be determined.



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    MedChemExpress tbm
    <t>TBM</t> <t>alleviated</t> <t>DOX-induced</t> cellular injury in H9c2 cells. (a, b) The chemical structures of DOX and TBM, respectively. (c, d) Viability of H9c2 cells treated with DOX and TBM for 24 h ( n = 6). (e) TBM improved the viability of DOX treated H9c2 cells ( n = 6), ns (not significant) versus the DOX group. (f–h) Levels of LDH, cTNT, and CK-MB in H9c2 cell media ( n = 4), ns (not significant) versus the CON group. Values indicate the mean ± standard deviation (SD). ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group.
    Tbm, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    TBM alleviated DOX-induced cellular injury in H9c2 cells. (a, b) The chemical structures of DOX and TBM, respectively. (c, d) Viability of H9c2 cells treated with DOX and TBM for 24 h ( n = 6). (e) TBM improved the viability of DOX treated H9c2 cells ( n = 6), ns (not significant) versus the DOX group. (f–h) Levels of LDH, cTNT, and CK-MB in H9c2 cell media ( n = 4), ns (not significant) versus the CON group. Values indicate the mean ± standard deviation (SD). ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM alleviated DOX-induced cellular injury in H9c2 cells. (a, b) The chemical structures of DOX and TBM, respectively. (c, d) Viability of H9c2 cells treated with DOX and TBM for 24 h ( n = 6). (e) TBM improved the viability of DOX treated H9c2 cells ( n = 6), ns (not significant) versus the DOX group. (f–h) Levels of LDH, cTNT, and CK-MB in H9c2 cell media ( n = 4), ns (not significant) versus the CON group. Values indicate the mean ± standard deviation (SD). ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Standard Deviation

    TBM attenuated inflammation in response to DOX treatment in vitro. (a–c) The relative mRNA levels of Il-6, Il-1 β , and Tnf -α in DOX treated H9c2 cells ( n = 5). (d–h) Western blotting assays of IL-6, IL-1 β , and TNF- α in each group ( n = 3). (i–k) Levels of IL-6, IL-1 β , and TNF- α in cell supernatant determined by ELISA ( n = 4). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM attenuated inflammation in response to DOX treatment in vitro. (a–c) The relative mRNA levels of Il-6, Il-1 β , and Tnf -α in DOX treated H9c2 cells ( n = 5). (d–h) Western blotting assays of IL-6, IL-1 β , and TNF- α in each group ( n = 3). (i–k) Levels of IL-6, IL-1 β , and TNF- α in cell supernatant determined by ELISA ( n = 4). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: In Vitro, Western Blot, Enzyme-linked Immunosorbent Assay

    TBM remarkably ameliorated DOX-evoked oxidative stress in H9c2 cells. (a, b) Flow cytometry was used to estimate the ROS levels in H9c2 cells ( n = 4). (c–e) The level of MDA and the activity of SOD and GSH-PX in H9c2 cells were detected by commercial kits ( n = 4). (f–h) The mRNA levels of Nrf2, Ho-1, and Nqo1 in H9c2 cells determined by qPCR ( n = 5). (i–m) Representative western blotting results for Nrf2, HO-1, and NQO1 in vitro ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM remarkably ameliorated DOX-evoked oxidative stress in H9c2 cells. (a, b) Flow cytometry was used to estimate the ROS levels in H9c2 cells ( n = 4). (c–e) The level of MDA and the activity of SOD and GSH-PX in H9c2 cells were detected by commercial kits ( n = 4). (f–h) The mRNA levels of Nrf2, Ho-1, and Nqo1 in H9c2 cells determined by qPCR ( n = 5). (i–m) Representative western blotting results for Nrf2, HO-1, and NQO1 in vitro ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Flow Cytometry, Activity Assay, Western Blot, In Vitro

    TBM protected H9c2 cells from DOX-induced apoptosis. (a, b) TUNEL staining labeled DNA breaks in H9c2 cells and its statistical analysis ( n = 3). (c, d) Flow cytometry was also used to evaluate the apoptosis of H9c2 cells ( n = 6). (e, f) Mitochondrial membrane potential (MMP) was determined by JC-1staining ( n = 3). (g, h) Flow cytometry was used to estimate MMP in each group ( n = 3). (i, j) Bax and Bcl-2 mRNA levels tested by qPCR ( n = 5). (k–o) The expression of BAX, BCL-2, and C-caspase3 at protein level determined by western blotting in vitro ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM protected H9c2 cells from DOX-induced apoptosis. (a, b) TUNEL staining labeled DNA breaks in H9c2 cells and its statistical analysis ( n = 3). (c, d) Flow cytometry was also used to evaluate the apoptosis of H9c2 cells ( n = 6). (e, f) Mitochondrial membrane potential (MMP) was determined by JC-1staining ( n = 3). (g, h) Flow cytometry was used to estimate MMP in each group ( n = 3). (i, j) Bax and Bcl-2 mRNA levels tested by qPCR ( n = 5). (k–o) The expression of BAX, BCL-2, and C-caspase3 at protein level determined by western blotting in vitro ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: TUNEL Assay, Staining, Labeling, Flow Cytometry, Membrane, Expressing, Western Blot, In Vitro

    TBM alleviated DOX-induced cardiotoxicity in mice. (a) Representative images of M-mode echocardiography in each group ( n = 6). (b, c) Statistical analysis of left ventricular ejection fraction (EF) and fractional shortening (FS) ( n = 6). (d) Heart rate of mice ( n = 6). (e) HE staining of mouse hearts ( n = 6). (f) The body weight changes in each group were recorded every other day ( n = 6). (g–i) The serum levels of LDH, cTNT, and CK-MB in mice ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM alleviated DOX-induced cardiotoxicity in mice. (a) Representative images of M-mode echocardiography in each group ( n = 6). (b, c) Statistical analysis of left ventricular ejection fraction (EF) and fractional shortening (FS) ( n = 6). (d) Heart rate of mice ( n = 6). (e) HE staining of mouse hearts ( n = 6). (f) The body weight changes in each group were recorded every other day ( n = 6). (g–i) The serum levels of LDH, cTNT, and CK-MB in mice ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Staining

    TBM inhibited DOX-induced inflammatory response in vivo. (a–c) The relative mRNA levels of Il-6, Il-1 β , and Tnf -α in mouse hearts (n = 6). (d–h) Western blotting for the detection of NF- κ B P65 and inflammatory factors (IL-6, IL-1 β , and TNF- α ) in mice ( n = 6). (i–k) The levels of IL-6, IL-1 β , and TNF- α in mouse hearts determined by ELISA ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM inhibited DOX-induced inflammatory response in vivo. (a–c) The relative mRNA levels of Il-6, Il-1 β , and Tnf -α in mouse hearts (n = 6). (d–h) Western blotting for the detection of NF- κ B P65 and inflammatory factors (IL-6, IL-1 β , and TNF- α ) in mice ( n = 6). (i–k) The levels of IL-6, IL-1 β , and TNF- α in mouse hearts determined by ELISA ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: In Vivo, Western Blot, Enzyme-linked Immunosorbent Assay

    TBM protected against DOX-induced oxidative stress in mice. (a, b) DHE staining indicated the generation of ROS in mice hearts ( n = 6). (c) The MDA levels in mouse hearts ( n = 6). (d, e) The activity of SOD and GSH-PX in mouse hearts ( n = 6). (f–h) The mRNA levels of Nrf2, Ho-1, and Nqo1 in mice determined by qPCR ( n = 6). (i–m) Western blotting analysis of Nrf2, HO-1, and NQO1 at the protein level ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM protected against DOX-induced oxidative stress in mice. (a, b) DHE staining indicated the generation of ROS in mice hearts ( n = 6). (c) The MDA levels in mouse hearts ( n = 6). (d, e) The activity of SOD and GSH-PX in mouse hearts ( n = 6). (f–h) The mRNA levels of Nrf2, Ho-1, and Nqo1 in mice determined by qPCR ( n = 6). (i–m) Western blotting analysis of Nrf2, HO-1, and NQO1 at the protein level ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Staining, Activity Assay, Western Blot

    TBM mitigated DOX-provoked cardiomyocyte apoptosis in vivo. (a, b) TUNEL staining represents cardiomyocyte apoptosis in the mouse hearts and its statistical result ( n = 6). (c, d) The mRNA levels of Bax and Bcl-2 determined by qPCR analysis ( n = 6). (e–i) Western blotting assays for the detection of BAX, BCL-2, and C-Caspase3 expression ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM mitigated DOX-provoked cardiomyocyte apoptosis in vivo. (a, b) TUNEL staining represents cardiomyocyte apoptosis in the mouse hearts and its statistical result ( n = 6). (c, d) The mRNA levels of Bax and Bcl-2 determined by qPCR analysis ( n = 6). (e–i) Western blotting assays for the detection of BAX, BCL-2, and C-Caspase3 expression ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: In Vivo, TUNEL Assay, Staining, Western Blot, Expressing

    TBM prevented DOX-evoked cellular damage by upregulating SIRT3 in H9c2 cells. (a, b) si-SIRT3 inhibited the expression of SIRT3 as determined by western blotting (n = 4). (c–h) The expression of SIRT3, P-P65, T-P65, IL-6, IL-1 β , and TNF- α was estimated by western blotting in H9c2 cells ( n = 3). (i–m) Western blotting was used to detect the expression of Nrf2, HO-1, and NQO1 in vitro ( n = 3). (n, p) si-Sirt3 partially reversed the inhibitory roles of TBM in DOX-induced ROS production ( n = 4). (o, q) Flow cytometry analysis demonstrated that SIRT3 inhibition blunted the beneficial effects of TBM on DOX-evoked apoptosis ( n = 6). (r–v) Western blotting was used to test the expression of apoptosis related proteins (BAX, BCL-2, and C-Caspase3) in H9c2 cells after si-Sirt3 treatment ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group; & P < 0.05 versus the DOX + TBM + siSIRT3 group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: TBM prevented DOX-evoked cellular damage by upregulating SIRT3 in H9c2 cells. (a, b) si-SIRT3 inhibited the expression of SIRT3 as determined by western blotting (n = 4). (c–h) The expression of SIRT3, P-P65, T-P65, IL-6, IL-1 β , and TNF- α was estimated by western blotting in H9c2 cells ( n = 3). (i–m) Western blotting was used to detect the expression of Nrf2, HO-1, and NQO1 in vitro ( n = 3). (n, p) si-Sirt3 partially reversed the inhibitory roles of TBM in DOX-induced ROS production ( n = 4). (o, q) Flow cytometry analysis demonstrated that SIRT3 inhibition blunted the beneficial effects of TBM on DOX-evoked apoptosis ( n = 6). (r–v) Western blotting was used to test the expression of apoptosis related proteins (BAX, BCL-2, and C-Caspase3) in H9c2 cells after si-Sirt3 treatment ( n = 3). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group; & P < 0.05 versus the DOX + TBM + siSIRT3 group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Expressing, Western Blot, In Vitro, Flow Cytometry, Inhibition

    SIRT3 inhibition alleviated the beneficial effects of TBM on DOX-induced cardiac injury in mice. (a, b) 3-TYP inhibited the expression of SIRT3 in mouse hearts ( n = 6). (c–h) The expression of SIRT3, P-P65, T-P65, IL-6, IL-1 β , and TNF- α evaluated by western blotting in mice ( n = 6). (i–m) Western blotting was used to examine the expression of Nrf2, HO-1, and NQO1 in mouse hearts ( n = 6). (n, o) DHE staining illustrated the generation of ROS after SIRT3 inhibition in mouse hearts ( n = 6). (p–s) Western blotting was used to detect the expression of the antiapoptotic protein BCL-2 and proapoptotic proteins (BAX and C-caspase3) in vivo ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group; & P < 0.05 versus the DOX + TBM+3-TYP group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

    doi: 10.1155/2023/9966355

    Figure Lengend Snippet: SIRT3 inhibition alleviated the beneficial effects of TBM on DOX-induced cardiac injury in mice. (a, b) 3-TYP inhibited the expression of SIRT3 in mouse hearts ( n = 6). (c–h) The expression of SIRT3, P-P65, T-P65, IL-6, IL-1 β , and TNF- α evaluated by western blotting in mice ( n = 6). (i–m) Western blotting was used to examine the expression of Nrf2, HO-1, and NQO1 in mouse hearts ( n = 6). (n, o) DHE staining illustrated the generation of ROS after SIRT3 inhibition in mouse hearts ( n = 6). (p–s) Western blotting was used to detect the expression of the antiapoptotic protein BCL-2 and proapoptotic proteins (BAX and C-caspase3) in vivo ( n = 6). Values indicate the mean ± SD. ∗ P < 0.05 versus the CON group and the TBM group; # P < 0.05 versus the DOX group; ns (not significant) versus the CON group; & P < 0.05 versus the DOX + TBM+3-TYP group.

    Article Snippet: DOX (#HY15142), TBM (#HY-N0890), and 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP, #HY108331) were purchased from MedChemExpress (New Jersey, USA); Dihydroethidium (DHE, #D1008) was obtained from Bioscience (Shanghai, China); the TdT-mediated dUTP nick end-labeling (TUNEL) assay kit (#C1088), Annexin V-FITC/PI (propidium iodide) apoptosis detection kit ( #C1062), Nuclear Protein Extraction Kit (#P0027), and mitochondrial membrane potential assay kit with JC-1 (#C2006) were purchased from Beyotime Biotechnology (Shanghai, China); assay kits for detecting lactate dehydrogenase (LDH, #A02022), creatine kinase isoenzymes (CK-MB, #E00611), cardiac isoform of Troponin T (cTnT, H1494), superoxide dismutase (SOD, #A0011) activity, glutathione peroxidase (GSH-PX, #A005), and malondialdehyde (MDA, #A0031) were purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China); the cell counting kit-8 (CCK8) was obtained from TopScience (Shanghai, China).

    Techniques: Inhibition, Expressing, Western Blot, Staining, In Vivo