线粒体通透性转换孔在锌缺乏模型大鼠心肌缺血/再灌注损伤中的作用  

Role of mitochondrial permeability transition pore in myocardial ischemia-reperfusion injury in rat models with zinc deficiency

作　　者：连婷 张瑞君 熊晓兰 张小雅 余涛 张世忠[1] LIAN Ting;ZHANG Rui-jun;XIONG Xiao-lan;ZHANG Xiao-ya;YU Tao;ZHANG Shi-zhong(Department of Physiology and Pathology, Medical Science Colloge of China Three Gorges University, Yichang 443002, China)

机构地区：[1]三峡大学医学院生理与病理学系,湖北宜昌443002

出　　处：《基础医学与临床》2022年第3期389-394,共6页Basic and Clinical Medicine

基　　金：国家自然科学基金(30872716);湖北省自然科学基金(2015CFB288);湖北省卫生与计划生育项目(WJ2015MB171)。

摘　　要：目的观察锌缺乏是否通过线粒体通透性转换孔(mPTP)对心肌缺血/再灌注(I/R)损伤发挥作用。方法通过饲喂锌缺乏饲料建立锌缺乏模型大鼠,将离体大鼠心脏全心缺血30 min,然后再灌注120 min,造成心肌I/R损伤模型。左心室插管检测心功能;分光光度法检测乳酸脱氢酶(LDH)活性;氯化三苯四氯唑(TTC)染色法检测心肌梗死面积;钙诱发线粒体肿胀法检测mPTP的开放程度。结果锌缺乏大鼠心肌梗死面积以及LDH释放增加(P<0.05),同时伴随左心室收缩功能降低(P<0.05)。与对照组相比,锌缺乏大鼠缺血前心脏线粒体的mPTP开放程度降低(P<0.05),但在缺血30 min后mPTP开放显著增加(P<0.05)。对照组和锌缺乏大鼠的心脏I/R损伤可通过抑制mPTP开放而明显减轻(P<0.01)。结论锌缺乏可通过增加心肌线粒体mPTP开放加重大鼠心肌I/R损伤。Objective To investigate whether zinc deficiency may induce myocardial ischemia-reperfusion(I/R)injury through mitochondrial permeability transition pore(mPTP).Methods The zinc-deficient rat model was established by feeding with a zinc-deficient fodder,myocardial I/R injury was induced with isolated rat hearts which were subjected to 30 min of global ischemia followed by 120 min of reperfusion.Left ventricular catheterization was used to detect cardiac function.The lactate dehydrogenase(LDH)was spectrophotometically measured;and 2,3,5-triphenyl-tetrazolium(TTC)staining method was applied to measure the area of myocardial infarction;Mitochondrial swelling induced by calcium was adapted as a method to examine the opening degree of mPTP.Results Rats with zinc deficiency showed an increased myocardial infarct size and LDH release(P<0.05),which was associated with a decreased recovery rate of left ventricular contractility(P<0.05).Compared to control rats,mPTP opening reduced in mitochondria of the heart of zinc-deficient rats before ischemia(P<0.05),but increased significantly after 30 min ischemia(P<0.05).The myocardial I/R injury in both control and zinc-deficient rats was significantlyattenuated by inhibition of mPTP opening(P<0.01).Conclusions Zinc deficiency may increase the myocardial I/R injury in rats through increase of mPTP opening.

关 键 词：锌缺乏症 心肌缺血/再灌注 线粒体通透性转换孔 

分 类 号：R363[医药卫生—病理学]