Simvastatin improves cardiac function in acute phase after myocardial infarction through Akt/eNOS pathway
10.3969/j.issn.1001-1978.2015.10.010
- VernacularTitle:辛伐他汀通过Akt/eNOS途径改善心肌梗死后急性期心功能
- Author:
Qiaoyan ZHU
;
Guangyu WANG
;
Yaguang BI
;
Qingyong ZHANG
;
Meng WEI
- Publication Type:Journal Article
- Keywords:
simvastatin;
myocardial infarction;
cardi-ac function;
oxidative stress;
acute phase;
p-Akt;
p-eNOS
- From:
Chinese Pharmacological Bulletin
2015;(10):1375-1378,1379
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of simvastatin ( Sim ) on endogenous antioxidant system after acute myocardial infarction ( AMI ) and its potential mecha-nisms. Methods The acute myocardial infarction ( AMI ) rat models were made by ligation left anterior descending of coronary artery. Then the successful models were randomly divided into myocardial infarc-tion group ( MI group) and simvastatin group ( Sim,20 mg·kg-1·d-1), another group without ligation left anterior descending of coronary artery served as sham group(Sham group). The Sim group was administered simvastatin by gavage for 7 days. MI group and Sham group received saline. Hemodynamic parameters, lipid levels, troponinI ( c-TnI ) and lactate dehydrogenase ( LDH) concentrations were examined after 7days, and the levels of superoxide dismutase ( SOD) and glutathi-one peroxidase ( GP) of myocardial antioxidant system were detected by ELISA. The expression of cardiac p-Akt and p-eNOS protein were detected by Western blot. Results Acute myocardial infarction significant-ly lowered cardiac hemodynamic parameters, increased serum c-TnI and LDH levels, lowered levels of SOD and GP, and lowered the expression of p-Akt and p-eNOS protein. However, Sim could effectively prevent the deterioration of cardiac function, reduce serum c-TnI and LDH levels, increase levels of SOD and GP, and increase p-Akt and p-eNOS protein expression. Conclusion Early using Sim can effectively improve heart function after acute myocardial infarction, acti-vate myocardial antioxidant system,and reduce myocar-dial necrosis, which may be related to increasing the expression of p-Akt and p-eNOS.
