中文摘要：

目的：探讨定心方对氧化应激所致心肌细胞凋亡的抑制作用及其可能作用机制。方法：培养乳鼠心肌细胞,采用200μMH2O2建立氧化应激损伤导致心肌细胞凋亡模型,运用Hoechest33324法测定心肌细胞凋亡情况,乙醛代谢法检测乙醛脱氢酶（ALDH2）活性,采用硫代巴比妥酸比色法、黄嘌呤氧化酶法分别测定心肌细胞中脂质过氧化产物丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性。结果：H2O2作用2h可导致心肌细胞凋亡,定心方显著抑制心肌细胞凋亡,表现为在Hoechest33324染色中,细胞核溶解和核碎裂减轻,凋亡细胞数明显减少（P〈0.05）,并且能够显著增强ALDH2及SOD活性,降低MDA含量（P〈0.05）。结论：定心方对H2O2所致的心肌细胞凋亡具有明显的抑制作用,其作用机制可能是通过抗脂质氧化及增强ALDH2酶活性而实现。

英文摘要：

Objective：To explore the inhibition mechanism of DingXin Recipe（DXR）on cardiomyocytes apoptosis induced by oxidative stress.Methods：Neonate rat cardiomyocytes were cultured with 200μM H2O2 to establish the cardiomyocyte apoptosis model induced by oxidative stress.Apoptosis was measured by Hoechest 33324 staining and ALDH2 activity was evaluated by the method of acetaldehyde metabolism.The content of malondialdehyde（MDA） was determined by measuring thiobarbituric acid-reactive substances and the activity of superoxide dismutase（SOD） was examined by xanthine oxidase method.Results：H2O2 would induce myocardium apoptosis after 2h,and the apoptosis was significantly decreased in thecells pretreated with DXR,and ALDH2 and SOD activity was significantly increased.However,the content of MDA was decreased.Conclusion ：DXR can exert inhibition activity on myocardium apoptosis induced by H2O2.The protective mechanism could be related to its ability to reduce lipid peroxidation and increase the activity of ALDH2 in cardiomyocytes.