乙醛脱氢酶2在大鼠心肌缺氧损伤中的抗凋亡作用

目的： 检测大鼠心肌在缺氧条件下发生细胞凋亡的变化，以及乙醛脱氢酶2（ALDH2）在此过程中所起的作用。 方法： 运用缺氧模型，比较大鼠心肌细胞在单独缺氧和经ALDH2特异性抑制剂daidzin预处理24 h后缺氧的凋亡改变，酶活性检测采用乙醛代谢法、凋亡的测定通过用Hoechest 33324、免疫荧光标记用流式细胞仪测定和TUNEL试剂盒检测。 结果： 心肌细胞在daidzin作用下，其酶活性被抑制而细胞无凋亡发生。在daidzin预处理24 h后再经缺氧诱导，比单独缺氧引起的心肌细胞凋亡更为明显：表现为在Hoechest 33324染色中，细胞核溶解和核碎裂(P<0.05)，FACS和TUNEL显示，凋亡细胞明显增加(P<0.05)。 结论： ALDH2酶活性降低可增加心肌细胞对缺氧导致凋亡的易感性，ALDH2对缺氧引起的细胞凋亡有拮抗作用。

Aldehyde dehydrogenase 2 prevents rat cardiomyocytes from apoptosis induced by hypoxia

AIM: To observe the effect of hypoxia on cardiaomyocytes apoptosis and the role of ALDH2 in the process. METHODS: Cultured cardiomyocytes of neonatal rats were used. Hypoxia was imposed to the cardiomyocytes with or without daidzin pretreatment. ALDH2 activity was measured by the method of acetaldehyde metabolism. Apoptosis was measured by Hoechest 33324 staining, fluorescence activated cell sorting (FACS) and the DeadEndTM fluorometric TUNEL system. RESULTS: ALHD2 enzyme activity in myocytes was inhibited by daidzin (24 h, 60 μmol/L) without induction of apoptosis. When exposed to hypoxia, however, the apoptisis was significantly increased in the cells pretreated with daidzin compared to those without the pretreatment. CONCLUSION: The reduction of ALDH2 activity might increase the susceptivity of myocytes to apoptosis following hypoxia, suggesting a protective role of ALDH2 in hypoxia-induced myocardial injury.