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目的:观察阿魏酸川芎嗪对大鼠心肌缺血再灌注损伤的影响,并探讨其可能的分子机制。方法:将60只雄性SD大鼠随机分成5组:假手术组、缺血再灌注组、川芎嗪(4 mg.kg-1)组、阿魏酸川芎嗪低剂量(4 mg.kg-1)组、阿魏酸川芎嗪高剂量(8 mg.kg-1)组;采用结扎左冠状动脉前降支30 min、再灌注120 min的方法复制大鼠心肌缺血再灌注模型;各组大鼠于再灌注前10 min分别颈iv给药;于再灌注结束后,进行血清生化学指标及心肌组织学检测。结果:阿魏酸川芎嗪能显著降低血清中肌酸激酶同功酶(CK-MB)、乳酸脱氢酶(LDH)和心肌钙蛋白I(cTnI)、丙二醛(MDA)的水平,提高总超氧化物歧化酶(T-SOD)活性,缩小心肌梗死范围,增加Bcl-2蛋白的表达,减少Bax蛋白的表达,降低Bcl-2/Bax的比值和心肌细胞凋亡指数,与缺血再灌注组比较,差异有统计学意义(P<0.01);阿魏酸川芎嗪部分指标优于川芎嗪(P<0.05),且呈现剂量依赖性。结论:阿魏酸川芎嗪对大鼠心肌缺血再灌注损伤具有良好保护作用;阿魏酸川芎嗪抗心肌细胞凋亡的机制可能与其上调Bcl-2基因和下调Bax基因表达有关。
Objective: To observe the effect of ligustrazine ferulate on myocardial ischemia-reperfusion injury in rats and to explore its possible molecular mechanism. Methods: Sixty male Sprague Dawley rats were randomly divided into 5 groups: sham operation group, ischemia-reperfusion group, ligustrazine (4 mg.kg-1) group, low dose of ligustrazine ferulate (4 mg.kg-1 ) Group and high dose of ligustrazine ferulate (8 mg.kg-1). The model of myocardial ischemia / reperfusion was established by ligating the left anterior descending coronary artery for 30 min and reperfusion for 120 min. Rats were given iv iv administration 10 min before reperfusion. Serum biochemical indexes and myocardial histological examination were performed after reperfusion. Results: Ligustrazine ferulate could significantly decrease the levels of CK-MB, LDH, cTnI and MDA, Total superoxide dismutase (T-SOD) activity, reduce the scope of myocardial infarction, increase the expression of Bcl-2 protein, reduce the expression of Bax protein, reduce the ratio of Bcl-2 / Bax and myocardial apoptosis index, and ischemia (P <0.01). Some indexes of tetramethylpyrazine ferulate were better than ligustrazine (P <0.05), and showed a dose-dependent manner. CONCLUSION: Ligustrazine ferulate has a good protective effect against myocardial ischemia-reperfusion injury in rats. Ligustrazine ferulate can inhibit the apoptosis of cardiomyocytes possibly through up-regulating Bcl-2 gene and down-regulating Bax gene expression.