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目的:研究芒果苷对柔红霉素所致大鼠心肌细胞毒性损伤影响及SIRT1介导的信号通路的变化。方法:取原代培养心肌细胞以4μmol/L柔红霉素建立心肌细胞损伤模型,以不同浓度芒果苷(25、50、100μmol/L)干预,选择白藜芦醇(25μmol/L)作为阳性对照药物,用RT-PCR方法检测SIRT1、FOXO3a、BIM的mRNA表达水平的变化,用免疫细胞化学染色法检测SIRT1、FOXO3a、BIM的蛋白水平的变化。结果:芒果苷作用于柔红霉素所致心肌损伤模型后,SIRT1 mRNA及蛋白的表达量有显著的提高,并且随着芒果苷浓度的增高,SIRT1的表达量逐渐增高;其下游因子FOXO3a与BIM mRNA及蛋白的表达量均显著降低,并呈一定量效关系。结论:芒果苷能改变柔红霉素所致心肌细胞损伤模型中SIRT1、FOXO3a、BIM的表达水平,提示SIRT1可能是芒果苷保护柔红霉素致心肌损伤模型的重要作用因子,并通过进一步调控且其下游FOXO3a和BIM两因子的表达来发挥保护损伤心肌的作用。
AIM: To study the effect of mangiferin on damaging myocardial cytotoxicity induced by daunorubicin and the change of SIRT1-mediated signaling pathway. Methods: Primary cultured cardiomyocytes were induced with 4μmol / L daunorubicin to establish cardiomyocyte injury models. Resveratrol (25μmol / L) was used as a positive control at different concentrations of mangiferin (25, 50 and 100μmol / L) Control drugs were detected by RT-PCR SIRT1, FOXO3a, BIM mRNA expression levels were detected by immunocytochemical staining SIRT1, FOXO3a, BIM protein levels. Results: The expression of SIRT1 mRNA and protein was significantly increased after the administration of mangiferin to daunorubicin-induced myocardial injury, and the expression of SIRT1 increased with the increase of mangiferin concentration. The downstream factors FOXO3a and BIM mRNA and protein expression were significantly reduced, and showed a certain dose-effect relationship. CONCLUSION: Mangiferin can change the expression levels of SIRT1, FOXO3a and BIM in daunorubicin-induced cardiomyocyte injury models, suggesting that SIRT1 may be an important factor in protecting myocardium induced by daunorubicin. Through further regulation And its downstream FOXO3a and BIM two factors play a role in protecting the injured myocardium.