贵州医科大学学报

2020, v.45;No.238(07) 805-810

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辅酶Q10对大鼠心肌缺血再灌注损伤的保护作用及机制
Protective Effect of Coenzyme Q10 on Myocardial Ischemia-Reperfusion Injury Rats and its Mechanism

李辉;张一娇;刘津军;卢静;孙莹莹;李燕燕;
LI Hui;ZHANG Yijiao;LIU Jinjun;LU Jing;SUN Yingying;LI Yanyan;Department of Cardiology,Handan Central Hospital;Department of Reproductive Medicine,Handan Central Hospital;

摘要(Abstract):

目的:探讨辅酶Q10(Co Q10)对大鼠心肌缺血再灌注(MI/R)损伤的保护作用及其机制。方法:60只Sprague Dawley(SD)大鼠随机均分为假手术组(sham组)、假手术+Co Q10组(Co Q10组)、模型组(Model组)及模型+Co Q10组(Model+Co Q10组),sham组和Co Q10组大鼠左冠状动脉前降支只穿线不结扎,Model组和Model+Co Q10组大鼠采用冠状动脉结扎手术法构建MI/R模型,造模后,Model+Co Q10组和Co Q10组大鼠肌肉注射Co Q10[10 mg/(kg·d)]、sham组和Model组肌肉注射等量的生理盐水,共7 d;记录第7天时各组大鼠心率,并抽取各组大鼠血液5 m L后处死大鼠取心肌组织,检测各组大鼠血清乳酸脱氢酶(LDH)、肌酸激酶(CK)及肌钙蛋白I(c Tn I)水平,计算各组大鼠的心肌梗死面积及观察心肌组织的病理学改变,检测大鼠心肌组织线粒体自噬相关分子蛋白细胞色素C氧化酶IV(COX IV)、Beclin-1、p62及自噬微管相关蛋白轻链3(LC3)的表达,透射电镜下观察大鼠心肌组织线粒体的形态学变化及自噬小体数量。结果:造模第7天时,与Sham组比较,Model组大鼠血清LDH、CK、c Tn I及心肌梗死面积均值均明显增加,心率明显降低(P <0. 01),大鼠心肌纤维排列紊乱、间隙增加,心肌组织COX IV、LC3、Beclin-1表达明显增加,p62表达明显降低(P <0. 05或P <0. 01),自噬小体数量增加;与模型组比较,Model+Co Q10组大鼠血清LDH、CK、c Tn I含量及心肌梗死面积均值均明显降低,心率均值明显升高(P <0. 05或P <0. 01),大鼠心肌纤维排列规则、间隙减小,心肌组织COX IV、LC3及Beclin-1表达明显降低,p62表达明显增加(P <0. 05或P <0. 01),自噬小体数量减少。结论:Co Q10可能通过抑制线粒体自噬而改善大鼠MI/R。
Objective: To explore the protective effect of coenzyme Q10( CoQ10) on myocardial ischemia-reperfusion( MI/R) injury in rats and its mechanism. Methods: Sixty Sprague Dawley( SD) rats were randomly divided into sham operation group( sham group),sham operation + CoQ10 group( CoQ10 group),model group( Model group) and model + CoQ10 group( Model + CoQ10 group). Sham group and CoQ10 group received the puncture of left anterior descending coronary( LAD) without ligation,the rats of Model group and Model + CoQ10 group were used to construct MI/R models by coronary artery ligation surgery. After modeling,Model + CoQ10 group and CoQ10 group were injected intramuscularly with CoQ10 [10 mg/( kg ·d) ],and Sam group and the model group was intramuscularly injected with the same amount of normal saline,for 7 days. The heart rates of of each group was recorded on the 7 thday. 5 m L of blood was drawn and then the myocardial tissues were taken from each group as the rats were executed. The levels of serum lactate dehydrogenase( LDH),creatine kinase( CK) and troponin I( cTnI) of the 4 groups were detected. The area of myocardial infarction and pathological change in each group were observed and calculated. The expressions of COX IV, Beclin-1, p62 and LC3 of mitochondrial autophagy-related molecular proteins in rat myocardial tissues were detected. Morphological changes in rat myocardium and mitochondria number autophagosome were observed by the transmission electron microscope. Results: On the 7 th day after rat modeling,compared with Sham group,the mean value of serum LDH,CK,cTnI and myocardial infarction area of the Model group significantly increased,but the mean value of heart rates was significantly reduced( P < 0. 01),and the myocardial fiber arrangement was disordered and the gap increased. The expression of myocardial tissues COX IV,LC3,Beclin-1 increased,p62 expression decreased( P < 0. 05 or P < 0. 01),and the number of autophagosomes increased. Compared with the model group,the serum contents of LDH,CK and cTnI in Model + CoQ10 group and the mean value of myocardial infarction area decreased,but the mean value of heart rates increased( P < 0. 05 or P <0. 01),and the arrangement of myocardial fibers and gaps were reduced; the expression of COX IV,LC3 and Beclin-1 in rat myocardial tissues decreased and p62 expression increased( P < 0. 05 or P <0. 01); the number of autophagosomes decreased. Conclusion: CoQ10 may improve MI/R in rats by inhibiting mitochondrial autophagy.

关键词(KeyWords): 线粒体;自噬;大鼠;辅酶Q10;心肌缺血再灌注;心肌损伤
mitochondria;autophagy;rats;coenzyme Q10(CoQ10);myocardial ischemiareperfusion(MI/R);myocardial injury

Abstract:

Keywords:

基金项目(Foundation): 河北省卫生和计划生育委员会科研基金项目(20181676)

作者(Author): 李辉;张一娇;刘津军;卢静;孙莹莹;李燕燕;
LI Hui;ZHANG Yijiao;LIU Jinjun;LU Jing;SUN Yingying;LI Yanyan;Department of Cardiology,Handan Central Hospital;Department of Reproductive Medicine,Handan Central Hospital;

Email:

DOI: 10.19367/j.cnki.2096-8388.2020.07.010

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