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目的 观察卡托普利对由外源性羟自由基诱导的心肌细胞凋亡有无影响。方法 ①利用第 4代心肌细胞 ,随机分成 15组 ,在终浓度为 10 -5mol/L、10 -4 mol/L、10 -3mol/L、10 -2 mol/L、10 -1mol/L的羟自由基无血清条件培养下分别共孵育 8h、16h、2 4h ,确定 10 -3 mol/L及 2 4h为诱导心肌细胞凋亡的最佳浓度及时间。②在上述条件下分别观察 3种不同浓度卡托普利 (10 -7mol/L、10 -6mol/L、10 -5mol/L)对心肌细胞存活率、形态学、DNA琼脂糖凝胶电泳及培养液中血管紧张素Ⅰ转换酶 (angiotensin convertingenzyme ,ACE)活性等参数的影响。结果 ①随着外源性羟自由基浓度升高、心肌细胞存活率明显降低 ,在外源性羟自由基终浓度为 10 -5～10 -3 mol/L范围内 ,随着浓度升高 ,培养液中ACE活性逐渐升高 ,但高于 10 -3 mol/L浓度时反而降低。② 10 -3 mol/L作用心肌细胞 2 4h心肌细胞凋亡程度最明显 ,在此条件下 ,加用卡托普利 (10 -7mol/L、10 -6mol/L、10 -5mol/L) ,心肌细胞存活率明显升高 ,培养液中ACE活性降低 ,心肌细胞凋亡程度降低 ,呈剂量依赖性。结论 卡托普利能减轻由外源性羟自由基诱导的乳鼠心肌细胞凋亡。
Objective To observe whether captopril has effect on cardiomyocyte apoptosis induced by exogenous hydroxyl radical. Methods ① The 4th generation cardiomyocytes were randomly divided into 15 groups and treated with 10 -5 mol / L, 10 -4 mol / L, 10 -3 mol / L, 10 -2 mol / L and 10 -1 mol / L Under the serum-free conditions, the cells were incubated for 8h, 16h and 24h respectively. The optimal concentration and time for inducing cardiomyocyte apoptosis were determined at 10 -3 mol / L and 24 h. ② Under the above conditions, the effects of three different concentrations of captopril (10 -7 mol / L, 10 -6 mol / L, 10 -5 mol / L) on cardiomyocyte survival, morphology, DNA agarose gel electrophoresis and The effect of angiotensin-converting enzyme (ACE) activity and other parameters in culture medium was studied. Results ① With the increase of exogenous hydroxyl radical concentration, the survival rate of cardiomyocytes significantly decreased. With the increase of exogenous hydroxyl radical concentration in the range of 10 -5 ~ 10 -3 mol / L, ACE activity in the fluid gradually increased, but higher than 10 -3 mol / L concentration decreased. (2) Cardiomyocytes apoptosis induced by 10-3 mol / L of cardiomyocytes was the most obvious. Under these conditions, captopril (10 -7 mol / L, 10 -6 mol / L, 10 -5 mol / L) , The survival rate of cardiomyocytes was significantly increased, ACE activity decreased in culture medium, myocardial apoptosis decreased in a dose-dependent manner. Conclusion Captopril can attenuate cardiomyocyte apoptosis induced by exogenous hydroxyl radicals.