自然科学版
陕西师范大学学报(自然科学版)
体育科学
间歇运动上调CTRP3表达抑制心梗大鼠心肌细胞凋亡及其机制
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候璐, 伏睿臻, 席悦, 田振军*
(陕西师范大学 体育学院, 陕西 西安 710119)
田振军,男,教授,博士生导师。E-mail:tianzj611@hotmail.com
摘要:
探讨间歇运动对心肌梗死(myocardial infarction, MI)大鼠C1q-肿瘤坏死因子相关蛋白3 (CTRP3)表征及心肌细胞凋亡的影响。3月龄雄性SD大鼠30只,随机选取8只为假手术对照组 (sham, S),S组只开胸穿线不结扎;余下大鼠永久性结扎左冠状动脉前降支,术后存活16只,随机分为心梗安静组(MI)和心梗+间歇运动组(ME),每组8只。ME组大鼠于术后1周进行为期8周的间歇运动训练,训练结束次日,腹腔麻醉取材。RT-qPCR检测CTRP3 mRNA水平,Western Blot检测心肌CTRP3、p-AKT、AKT、p-mTOR、mTOR、细胞色素C、Bcl-2、Bax、BNP蛋白表达,TUNEL法检测心肌细胞凋亡,Masson染色分析心肌胶原容积(collagen volume fraction, CVF)百分比,血流动力学方法评定心功能。研究发现:心梗后大鼠心功能显著降低,心肌纤维化水平显著增加,CTRP3 mRNA表达显著升高,蛋白表达显著降低,AKT和mTOR蛋白磷酸化上调,细胞色素C表达显著升高,Bcl-2/Bax比值降低,TUNEL阳性颗粒增加,BNP蛋白表达上调。间歇运动可显著改善心梗大鼠心功能,降低心肌纤维化水平,CTRP3基因与蛋白表达都显著升高,进一步上调AKT和mTOR蛋白磷酸化,降低细胞色素C蛋白表达,升高Bcl-2/Bax比值,减少TUNEL阳性颗粒,下调BNP的蛋白表达。间歇运动可升高心梗大鼠心肌中CTRP3水平,激活AKT/mTOR通路,抑制心肌细胞凋亡,改善心梗心脏病理性重塑,提高心功能。
关键词:
间歇运动; 心肌梗死; 细胞凋亡; CTRP3
收稿日期:
2016-11-15
中图分类号:
G804.4
文献标识码:
A
文章编号:
1672-4291(2017)03-0112-07doi:10.15983/j.cnki.jsnu.2017.03.234
基金项目:
国家自然科学基金(31371199,31171141)
Doi:
Interval exercise training up-regulates CTRP3 expression and inhibits cardiomyocyte apoptosis in rat with myocardial infarction
HOU Lu, FU Ruizhen, XI Yue, TIAN Zhenjun*
(School of Physical Education, Shaanxi Normal University, Xi′an 710119, Shaanxi, China)
Abstract:
This study was carried out to detect the effects of interval exercise training on cardiomyocyte apoptosis and the expression of C1q/tumor necrosis factor-related protein-3(CTRP3) in rat with myocardial infarction(MI).Adult male sprague-dawley rats, 3-mouth old, were randomly divided into three groups: Sham-operated group (Sham), sedentary MI group (MI) and MI with interval exercise group (ME). The MI model was established by ligation of the left anterior descending coronary artery, and rats in ME were subjected to 8 weeks of interval exercise training. Cardiac function, heart tissue remodeling and cardiomyocyte apoptosis were evaluated after the training. The expression of CTRP3, p-AKT, AKT, p-mTOR, mTOR, Cytochrome C, Bcl-2, Bax and BNP was determined in the peri-infarcted area of the left ventricle by Western Blot or RT-qPCR.MI resulted in cardiac dysfunction and myocardial fibrosis, increased the mRNA expression of CTRP3 and reduced its protein expression, activated the phosphorylation of Akt and mTOR, induced cardiomyocyte apoptosis and up-regulated the BNP protein expression. Compared with MI group, interval exercise training significantly improved cardiac function, attenuated myocardial remodeling by reducing CVF%, up-regulated the CTRP3 expression and phosphorylation of Akt and mTOR, and inhibited cardiomyocyte apoptosis in MI rats.Interval exercise training up-regulated CTRP3 expression, activated Akt/mTOR signaling in infarcted heart, inhibited cardiomyocyte apoptosis, and improved cardiac function.
KeyWords:
interval exercise training; myocardial infarction; cardiomyocyte apoptosis; CTRP3