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目的研究吡咯列酮对糖尿病大鼠心脏缺血再灌注的保护作用及机制。方法链脲佐菌素腹腔注射建立糖尿病大鼠模型,将糖尿病大鼠45只随机分为5组:假手术组,缺血再灌注组,吡格列酮5 mg/kg组,吡格列酮10 mg/kg组和吡格列酮20 mg/kg组,每组9只,利用体内结扎左前降支的方法建立缺血再灌注损伤模型,取大鼠心肌组织,检测细胞凋亡、丙二醛(MDA)、超氧化物歧化酶(SOD)、Bax、Bcl-2、Cytochrome c和Smac/DIABLO和半胱氨酸天冬酶9、3(Caspase 9、3)的变化。结果与缺血再灌注组相比,吡格列酮5、10和20 mg/kg可呈剂量依赖性减少MDA含量、Bax蛋白表达、Caspase 9、3酶活性,增加SOD酶活性和Bc-l2蛋白表达,抑制细胞凋亡。结论吡格列酮预处理可降低糖尿病大鼠心肌缺血再灌注后细胞的氧化损伤水平,下调线粒体凋亡蛋白表达,减少心肌细胞凋亡数以起到心肌保护作用。
Objective To study the protective effect and mechanism of pioglitazone on myocardial ischemia / reperfusion in diabetic rats. Methods Diabetic rats were induced by streptozotocin. 45 diabetic rats were randomly divided into 5 groups: sham-operated group, ischemia-reperfusion group, pioglitazone 5 mg / kg group and pioglitazone 10 mg / kg group Pioglitazone 20 mg / kg group, 9 rats in each group. The model of ischemia-reperfusion injury was established by ligation of the left anterior descending artery in vivo. The myocardial tissue was taken and the apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD), Bax, Bcl-2, Cytochrome c and Smac / DIABLO and Caspase 9,3. Results Compared with ischemia-reperfusion group, pioglitazone at 5, 10 and 20 mg / kg decreased MDA content, Bax protein expression, Caspase 9,3 activity, SOD activity and Bc-l2 protein expression in a dose- Inhibit apoptosis. Conclusion Pioglitazone preconditioning can reduce myocardial oxidative damage, decrease the expression of mitochondrial apoptosis protein and decrease the number of cardiomyocyte apoptosis in myocardial ischemia-reperfusion of diabetic rats.