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目的探讨黄嘌呤氧化酶(xanthine oxidase,XO)抑制剂别嘌呤醇对心肌梗死大鼠心肌细胞凋亡的影响。方法结扎冠脉前降支制作大鼠心肌梗死模型,随机分为假手术组(sham,n=5),心肌梗死组(MI,n=16)和别嘌呤醇组(50 mg.kg-1.d-1,n=15),28 d后检测心肌梗死面积,TUNEL法检测心肌细胞凋亡,免疫组化法检测Fas蛋白表达,Western blot检测XO和caspase 3蛋白表达,比色法测定XO和清除活性氧活力。结果MI组非梗死区心肌细胞凋亡指数升高,Fas、XO、caspase 3蛋白表达增强,XO活力增加,清除活性氧活力降低(P<0.01);别嘌呤醇组明显缓解了上述指标的变化。结论别嘌呤醇能够抑制非梗死区心肌细胞凋亡,其作用机制可能与减少活性氧生成及降低Fas和caspase 3的表达有关。
Objective To investigate the effect of xanthine oxidase (XO) inhibitor allopurinol on cardiomyocyte apoptosis in myocardial infarction rats. Methods The model of myocardial infarction was established by ligating the anterior descending coronary artery in rats. The rats were randomly divided into sham operation group (n = 5), myocardial infarction group (MI, n = 16) and allopurinol group (50 mg.kg-1 .d-1, n = 15). The area of myocardial infarction was detected 28 days later. Cardiomyocyte apoptosis was detected by TUNEL. The expression of Fas protein was detected by immunohistochemistry. The protein expressions of XO and caspase 3 were detected by Western blot. And remove reactive oxygen species. Results The apoptotic index of myocardial cells in non-infarcted area increased, the expression of Fas, XO and caspase 3 increased, the activity of XO increased and the activity of reactive oxygen species (ROS) decreased (P <0.01). Allopurinol group alleviated the changes of above indexes . Conclusion Allopurinol can inhibit cardiomyocyte apoptosis in non-infarcted area, and its mechanism may be related to the reduction of reactive oxygen species generation and the decrease of Fas and caspase 3 expression.