心梗大鼠通过有氧运动激活PI3K-Akt-PKG-1/p-PLN-SERCA2a通路抑制心肌细胞凋亡改善心功能  

Aerobic-exercise-induced Activation of PI3K-Akt-PKG-1/p-PLN-SERCA2a Pathway Inhibits Myocardial Cell Apoptosis and Improves Cardiac Function in Myocardial Infarction Rats

作　　者：刘纽 田振军[1,2] LIU Niu;TIAN Zhen-Jun(School of Physical Education,Weinan Normal University,Weinan 714099,China;Institute of Sports and Exercise Biology,School of Physical Education,Shaanxi Normal University,Xi'an 710119,China)

机构地区：[1]渭南师范学院体育学院,渭南714099 [2]陕西师范大学体育学院暨运动生物学研究所,西安710119

出　　处：《生物化学与生物物理进展》2021年第6期698-708,共11页Progress In Biochemistry and Biophysics

基　　金：陕西省科技厅科研计划项目(2021JQ-827);陕西省教育厅科研计划项目(20JK0633)资助。

摘　　要：为探讨有氧运动对心梗大鼠心功能的影响,将3月龄SD雄性大鼠适应性喂养1周后随机分为正常组(C组)、假手术组(S组)、心梗安静组(MI组)、正常+运动组(CE组)、心梗+运动组(ME组),每组8只.MI组结扎左冠状动脉前降支制备心梗模型;S组只穿线不结扎;CE组与ME组术后1周开始有氧训练,运动方式为依次以10 m/min×10 min,13 m/min×10 min,16 m/min×40 min进行跑台训练,60 min/d,每周5 d,连续4周.训练结束后次日,采用血流动力学检测左室收缩压(left ventricular systolic pressure,LVSP)、左室舒张末压(left ventricular end-diastolic pressure,LVEDP)和收缩/舒张速率(±dp/dtmax)等心功能相关指标,单细胞可视化动缘探测系统(IonOptix)测定[Ca^(2+)]i变化百分数([Ca^(2+)]iamplitude)、[Ca^(2+)]i荧光比率(ratio)、达峰速率(departure velocity)、达峰时程(time to peak,TTP)、达峰50%时程(time to peak50%,TTP50%)、达基线50%时程(time to baseline50%,TTB50%)、达基线速率(return velocity)以及ratio改变幅度(ratio amplitude)等钙瞬变指标和肌节最大收缩及舒张速率(±dl/dtmax)、肌节长度(sarcomere length,SL)、肌节收缩幅度(peak twitch amplitude,PTA)、肌节缩短分数(SL shortening%)等心肌细胞收缩指标,蛋白质印迹(Western blotting)方法检测PI3K-Akt-PKG-1/p-PLN-SERCA2a信号通路及细胞凋亡相关蛋白.与S组相比,MI组PI3K-Akt-PKG-1/p-PLNSERCA2a信号通路被显著抑制,心肌细胞凋亡显著增加,LVEDP显著升高,LVSP和±dp/dtmax显著降低,[Ca^(2+)]i amplitude、ratio amplitude、departure velocity和return velocity均显著下降,TTB50%、TTP和TTP50%均显著增加,心肌细胞SL shortening%、PTA、±dl/dtmax均显著减少;与MI组相比,ME组PI3K-Akt-PKG-1/p-PLN-SERCA2a信号通路显著被激活,细胞凋亡显著被抑制,LVEDP显著降低,LVSP和±dp/dtmax显著升高,ratio amplitude、[Ca^(2+)]iamplitude、ratio velocity和departure velocity均显著提高,TB50%、TTP和TTP50%均显著缩短,心肌细胞SL ShorteTo investigate the effect of aerobic exercise on cardiac function in myocardial infarction rats,SD male rats were randomly divided into normal group(C group),sham operation group(S group),myocardial infarction group(MI group),normal+exercise group(CE group)and myocardial infarction+exercise group(ME group)after 1 week of adaptive feeding.Then,an MI model was established by ligating the left anterior descending coronary artery and group S only threading without ligation.One week after surgery,animals were randomly assigned to receive 4 weeks of no training or training(1 h/d,5 d/week on a treadmill).In detail,the training consisted of two 10-minute sessions at speed of 10 m/min and 13 m/min,and the remaining 40 min at speed of 16 m/min.The next day after the training,blood flow mechanics was used to detect cardiac function.A single cell visual moving edge detection system(Ion Optix)was used to determine[Ca^(2+)]iamplitude,[Ca^(2+)]ifluorescence ratio,departure velocity,time to peak(TTP),time to peak 50%(TTP50%),time to baseline 50%(TTB50%),return velocity,ratio amplitude,maximum contraction and diastolic rate of sarcomere(±dl/dtmax),sarcomere length(SL),peak twitch amplitude(PTA)and SL shortening%.The related proteins of PI3K-AKT-PKG-1/p-PLN-SERCA2a signaling pathway and apoptosis were detected by PI3K-AKT-PKG-1/p-PLN-SERCA2a signaling pathway and apoptosis related proteins were detected by Western blotting.Compared with group S,in group MI,PI3K-Akt-PKG-1/pPLN-SERCA2a signaling pathway is significantly inhibited,apoptosis and left ventricular end-diastolic pressure(LVEDP)are significantly increased,left ventricular systolic pressure(LVSP)and maximum pressure increasing and decreasing rate(±dp/dtmax),[Ca^(2+)]iamplitude,[Ca^(2+)]iratio amplitude,departure velocity and return velocity all significantly reduce,and TTB50%,TTP and TTP50%both significantly increase.The myocardial cells were significantly reduced at the SL shortening%,PTA,±dp/dtmax.Compared with MI group,PI3K-Akt-PKG-1/pPLN-SERCA2a signaling pathway in

关 键 词：信号通路 心肌梗死 有氧运动 大鼠 

分 类 号：G804.2[文化科学—运动人体科学]