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目的探究洛伐他汀预处理对急性心脏缺血再灌注心肌细胞凋亡的影响。方法将24只SD大鼠随机均分为3组模型对照组(C);洛伐他汀(Lovastatin)组(L),胃管直接灌注洛伐他汀每天15mg/kg,2周;洛伐他汀L-硝基精氨酸甲酯(L-NAME)组(N),洛伐他汀每天15mg/kg直接灌胃同时腹腔注射L-NAME30mg/kg,2周。2周后建立在体急性缺血再灌注心脏模型,观察洛伐他汀对缺血再灌注前、后心肌细胞Bcl-2、Bax凋亡相关蛋白表达以及心肌细胞凋亡的影响。结果各组血脂指标差异无统计学意义,洛伐他汀上调心肌细胞内Bax凋亡相关蛋白表达(P<0.05),对Bcl-2凋亡相关蛋白影响不明显(P>0.05);明显降低缺血再灌注心肌细胞凋亡指数(P<0.05)。结论洛伐他汀有效减少心脏缺血再灌注后心肌细胞凋亡,具有非降脂的延迟性心肌保护作用。其抗凋亡作用不受抑制一氧化氮合酶(NOS)活性和改变心肌细胞内凋亡相关蛋白Bax表达影响,具体机制须进一步实验探究。
Objective To investigate the effect of lovastatin preconditioning on cardiomyocyte apoptosis in acute cardiac ischemia-reperfusion. Methods Twenty-four Sprague-Dawley rats were randomly divided into three groups: model control group (C), Lovastatin group (L), gastric tube with lovastatin 15 mg / kg daily for 2 weeks, lovastatin L - L-NAME group (N), lovastatin 15mg / kg per day by intragastric administration of L-NAME 30mg / kg, 2 weeks. After 2 weeks, we established the model of acute ischemia-reperfusion heart and observed the effect of lovastatin on the expression of Bcl-2 and Bax apoptosis-related protein and cardiomyocyte apoptosis in myocardial cells before and after ischemia / reperfusion. Results There was no significant difference in serum lipids between each group. Lovastatin increased the expression of apoptosis related protein (Bax) in cardiomyocytes (P <0.05), but had no effect on Bcl-2 related protein (P> 0.05) Apoptosis index of cardiomyocytes after blood reperfusion (P <0.05). Conclusion Lovastatin can effectively prevent cardiomyocyte apoptosis after myocardial ischemia and reperfusion, and has a non-lipid-lowering and delayed myocardial protective effect. Its anti-apoptotic effect was not inhibited by inhibiting the activity of nitric oxide synthase (NOS) and altering the expression of apoptosis-related protein Bax in cardiomyocytes. The specific mechanism needs to be explored further.