首页 | 本学科首页   官方微博 | 高级检索  
     

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
引用本文:刘纽,田振军. 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[J]. 生物化学与生物物理进展, 2021, 48(6): 698-708
作者姓名:刘纽  田振军
作者单位:2)陕西师范大学体育学院暨运动生物学研究所,西安 710119,2)陕西师范大学体育学院暨运动生物学研究所,西安 710119
基金项目: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[Ca2+]i变化百分数([Ca2+]iamplitude)、[Ca2+]i荧光比率(ratio)、达峰速率(departure veloc...

关 键 词:信号通路  心肌梗死  有氧运动  大鼠
收稿时间:2020-10-24
修稿时间:2020-12-14

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
LIU Niu and TIAN Zhen-Jun. 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[J]. Progress In Biochemistry and Biophysics, 2021, 48(6): 698-708
Authors:LIU Niu and TIAN Zhen-Jun
Affiliation:2)Institute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi''an 710119, China,2)Institute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi''an 710119, China
Abstract:To 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 [Ca2+]i amplitude, [Ca2+]i fluorescence ratio, departure velocity, time to peak(TTP), time to peak50%(TTP50%), time to baseline50%(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/p-PLN-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), [Ca2+]i amplitude, [Ca2+]i ratio 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/p-PLN-SERCA2a signaling pathway in ME group is significantly activated, apoptosis and LVEDP are significantly reduced, LVSP and ±dp/dtmax are significantly increased, ratio amplitude, [Ca2+]i amplitude, ratio velocity and departure velocity are significantly increased, and TB50%, TTP and TTP50% are significantly shortened. The myocardial cells were significantly inaeased at the SL shortening%, PTA, ±dp/dtmax. It can be concluded that aerobic exercise improves the calcium transient and myocardial systolic function in peripheral infarction area of MI rats, activates the PI3K-Akt-PKG-1/p-PLN-SERCA2a signal, inhibits the apoptosis of myocardial cells, and improves myocardial infarction function. Moreover, the improvement of myocardial infarction function is closely related to the activation of PI3K-Akt-PKG-1/p-PLN-SERCA2a signaling pathway and the inhibition of myocardial cell apoptosis.
Keywords:signaling pathway  myocardial infarction  aerobic exercise  rats
本文献已被 CNKI 等数据库收录!
点击此处可从《生物化学与生物物理进展》浏览原始摘要信息
点击此处可从《生物化学与生物物理进展》下载全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号