Effect of Losartan on Myocardial Remodeling in Myocardial Infarction Rats’Model
10.3969/j.issn.1000-3614.2014.08.018
- VernacularTitle:氯沙坦影响大鼠心肌梗死后心室重塑的机制研究
- Author:
Zhenyu CUI
;
Suxia HAN
;
Lei FENG
;
Xiaoguang DONG
;
Liping GUO
;
Jianmei CHANG
- Publication Type:Journal Article
- Keywords:
Angiotensin converting enzyme2;
Myocardial infarction;
Angiotensin II;
Myocardial remodelling;
Losartan
- From:
Chinese Circulation Journal
2014;(8):629-633
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of losartan on angiotensin II (Ang II) expression and myocardial remodeling in myocardial infarction (MI) rats’ model.
Methods: A total of 32 SD male rats were divided into 4 groups, Sham operation group, MI group, MI with losartan 10mg/(kg·d) group and MI with losartan 20mg/(kg·d). n=8 in each group. MI model was established and the electrocardiogram changes before and after MI were recorded, hemodynamic indexes were detected at 4 weeks after MI, pathological changes of myocardial tissue were examined by HE staining. The myocardial mRNA and protein expressions of ACE2 and Ang II were detected by RT-PCR and Western Blot analysis.
Results: Compared with Sham operation group, MI group showed increased LVMI and decreased LVEF P<0.05;the above changes were getting better in both MI with losartan groups in a dose-dependent manner. The pathological examination presented that MI group had myocardial cell swelling, fracture, hyperplasia and inflammatory cell infiltration, those damages were less in MI with losartan groups in a dose-dependent manner, Sham operation group had no pathological changes. Compared with Sham operation group, the mRNA and protein expressions of Ang II were obviously higher in MI group, P<0.05 and the expressions were decreased in MI with losartan groups in a dose-dependent manner;the mRNA and protein expressions of ACE2 were slightly increased in MI group and the expressions were further increased in MI with losartan groups in a dose-dependent manner.
Conclusion: Losartan could increase ACE2 expression and therefore, inhibit Ang II expression and improve the ventricular remodeling in MI rats’ model.
