Protective effect of swimming on myocardial infarction:Role of AMPK/PGC-1alpha pathway
Objective:To investigate the effect of swimming(SW)on myocardial infarction(MI)injury by regulating the AMPK/PGC-1α pathway in mice.Methods:A myocardial infarction model was in-duced in mice by ligation of the left anterior descending coronary artery.The mice were randomly di-vided into four groups(n=15):Sham group(Sham),MI group,MI+SW group(MI+SW),and MI+SW+AMPK inhibitor Compound c group(MI+SW+CC).The swimming exercise groups were given none-load swimming training for 9 weeks.The left ventricular pressure,the rate of maxi-mal left ventricular pressure increase(+dp/dtmax),and the rate of maximal left ventricular pressure de-crease(-dp/dtmax)were measured.Myocardial structure and fibrosis were observed by HE and Mas-son's staining.The apoptosis rate,lactate dehydrogenase(LDH)creatine kinase isoenzyme(CK-MB)activities,and troponin Ⅰ(cTnⅠ)content were observed.The reactive oxygen species(ROS)level,su-peroxide dismutase(SOD)activity,malondialdehyde(MDA)content,and mitochondrial ATP con-tent were assayed too.Western Blot was used to detect the expression of Cleaved caspase-3,Cyto-chrome c,p-AMPK,p-ACC,and PGC-1α.Results:Compared with that in the Sham group,the left ventricular pressure and ±dp/dtmax in the MI group was significantly decreased.Myocardial fiber ar-rangement was disordered and ruptured.Myocardial fibrosis,the apoptosis rate,LDH and CK-MB activities,and cTnⅠ content were also increased.The ROS level,MDA content,and mitochondrial ATP content were increased as well as SOD activity was decreased.In addition,the expression of p-AMPK,p-ACC,and PGC-1α was decreased,while the expression of cleaved caspase-3 and cyto-chrome c was increased.Compared with that in the MI group,the left ventricular pressure and ±dp/dtmax in the MI+SW group was significantly increased.Myocardial fiber arrangement,fibrosis,apoptosis rate,LDH and CK-MB activities,and cTnⅠ content were alleviated.The ROS level,MDA content,and mitochondrial ATP content were decreased as well as SOD activity was in-creased.The expression of p-AMPK,p-ACC,and PGC-1α was increased.Compound c could block the effect of swimming on MI-induced myocardial injury and the AMPK/PGC-1α pathway after myo-cardial infarction.Conclusion:Swimming could alleviate cardiac injury after myocardial infarction by inhibiting oxidative stress and improving mitochondrial energy metabolism via the AMPK/PGC-1αpathway in mice.
NETL
NSTL
万方数据
