三七总皂对氧化应激所致心肌细胞凋亡的抑制机制

目的 探讨三七总皂苷对氧化应激所致心肌细胞凋亡的抑制机制。方法培养乳鼠心肌细胞，采用40μM H2O2建立氧化应激损伤导致心肌细胞凋亡模型，使用流式细胞仪检测心肌细胞凋亡情况，运用westernblot检测caspase3、Cytochromec在细胞内的表达。结果H2O2作用5h可导致心肌细胞凋亡，三七总皂苷显著抑制心肌细胞凋亡，对照组、模型组和试验组凋亡率分别为（3．58±0．53）％、（26．34±3．00）％、（9．89±1．64）％，并能明显抑制caspase3、CytochromeC在细胞内的表达，对照组、模型组和试验组caspase3表达指数分别为8．48±1．36、41．51±4．68、9．86±1．56，对照组、模型组和试验组Cytochrome c表达指数分别为8．63±0．52、46．06±3．53、10．40±1．12。结论三七总皂苷对H2O2所致的心肌细胞凋亡具有明显的抑制作用，其作用机制可能是减少Cytochromec释放，抑制心肌细胞内caspase 3表达。

The inhibition mechanism of Panax notoginsenosides (PNS) on cardiomyecytes apoptosis induced by oxidative stress

Objective To explore the inhibition mechanism of Paaax notoginsenosides （PNS）on eardiomyocytes apoptosis indhced by oxidative stress. Methods Neonate rat cardiomyocytes were cultured with 40μ M H2O2 to establish the cardiomyocyte apoptosis model induced by oxidative stress and the protective effects of PNS on myocardium apoptosis determined by flow cytometry （FCM）,and assayed the expression of caspase 3 and cytochrome c by western blot. Results H2O2 would induce myocardium apoptosis after 5h, but PNS could obviously inhibit cardiomyocyte apoptosis, and the rate of control,model and test group was 3.58±0.53% ,26.34±3.00% and 9.89±1.64% respectively. Additionally PNS could inhibit the expression of caspase 3 and cytochrome c in cardiomyocytes,the caspase 3 expression index of control,model and test group was 8.48±1.36,41.51±4.68 and 9.86±1.56 respectively,and that of cytochrome c was 8.63±0.52,46.06±3.53 and 10.40±1.12 respectively. Conclusion PNS can exert inhibition activity on myocardium apeptosis induced by H2O2 and its protective mechanism might be that it could reduce the release of cytochrome c and inhibit the expression of caspase 3 in cardiomyocytes.