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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40μМH2O2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western blot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Cytochromec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caspase3表达。
Objective To investigate the inhibitory mechanism of panax notoginseng saponins on cardiomyocyte apoptosis induced by oxidative stress. Methods Cardiomyocytes from neonatal rats were cultured and 40 μM H2O2 was used to establish a model of cardiomyocyte apoptosis induced by oxidative stress. Flow cytometry was used to detect cardiomyocyte apoptosis. Western blot was used to detect the expression of caspase3 and Cytochromec in the cells. RESULTS: H2O2 treatment resulted in apoptosis of cardiomyocytes for 5 h. Panax notoginseng saponins significantly inhibited cardiomyocyte apoptosis. Apoptosis rates in control, model and experimental groups were (3.58±0.53)%, (26.34±3.00)%, respectively. The expression of caspase3 and Cytochromec was significantly inhibited in the cells. The expression indexes of caspase3 in the control, model and experimental groups were 8.48±1.36, 41.51±4.68, and 9.86±1.56, respectively. The control group, model group and The Cytochromec expression index of the test group was 8.63±0.52, 46.06±3.53, and 10.40±1.12, respectively. Conclusion Panax notoginseng saponins can obviously inhibit the apoptosis of cardiomyocytes induced by H2O2. The mechanism may be to reduce the release of Cytochromec and inhibit the expression of caspase3 in cardiomyocytes.