运动预处理对大鼠心脏缺血再灌注损伤的保护作用

Effect of exercise preconditioning on myocardial ischemia reperfusion injury in rats

目的:探讨运动预处理对心脏缺血再灌注损伤的保护作用及可能机制。方法:雄性成年SD大鼠40只,随机分为4组,每组10只:对照组、运动预处理组、缺血再灌注组、运动预处理+缺血再灌注组,运动预处理组、运动预处理+缺血再灌注组进行6周的中等强度跑台运动。建立在体心脏缺血再灌注(缺血30 min,再灌注120min)模型;检测血清中c Tn I、LDH的含量,HE染色观察心肌纤维结构的变化,Western blot检测心肌组织中Cleaved Caspase-3、Cytochrome C、Sirt1和Ac-FOXO1蛋白的表达,测定心肌线粒体SOD活性和MDA含量。结果:运动预处理组和对照组相比,各项指标差异均无统计学意义(P均>0.05);心肌缺血再灌注后,血清中LDH和c Tn I含量升高,心肌纤维结构出现断裂,凋亡相关蛋白Cleaved Caspase-3、Cytochrome C表达增加,SOD活性下降,MDA含量增加,Sirt1蛋白表达减少,FOXO1乙酰化增加(P均<0.05);而运动预处理可明显改善心肌缺血再灌注引起的LDH和c Tn I升高,减少心肌纤维断裂,下调凋亡相关蛋白Cleaved Caspase-3、Cytochrome C的表达,增加SOD活性,降低MDA含量,上调Sirt1蛋白的表达,减少FOXO1的乙酰化(P均<0.05)。结论:运动预处理对心肌缺血再灌注损伤具有保护作用,这种保护作用可能是通过上调Sirt1的表达,从而降低心肌氧化应激损伤实现的。

Aim： To investigate the role and underlying mechanism of exercise preconditioning（ EP） on myocardial ischemia reperfusion（ IR）. Methods： Forty male SD rats were randomly allocated into 4 groups（ n = 10）,namely the control,EP,IR,EP ＋ IR groups. The rats in EP and EP ＋ IR groups were conducted middle intensity exercises for six weeks,the ischemia（ 30 min） reperfusion（ 120 min） model was induced by occlusion of left anterior descending branch of coronary artery. Serum lactate dehydrogenase（ LDH） and c Tn I were determined. The morphological changes in myocardial fiber were analyzed by HE staining. Western blot was used to determine the expressions of Cleaved Caspase-3,Cytochrome C,Sirt1 and Ac-FOXO1. The activity of superoxide dismutase（ SOD） and the content of malondialdehyde（ MDA） were measured.Results： Compared with control group,EP had no effect on normal hearts（ P〈0. 05）. The hearts in IR group exhibited increases in the content of LDH,c Tn I,MDA,the expression of Cleaved Caspase-3,Cytochrome C,and the expression of Ac-FOXO1,and decreases in the activity of SOD and the expression of Sirt1（ P〈0. 05）. The hearts of EP ＋ IR group were significantly attenuated the above effects induced by IR（ P〈0. 05）. Conclusion： EP could alleviate IR-induced heart injury partly via upregulating Sirt1 and finally reduce the oxidative stress injury.