Protective Roll of Atorvastatin on Cardiac Remodeling Induced by Pressure Overload in Experimental Mice With its Mechanism
10.3969/j.issn.1000-3614.2015.11.014
- VernacularTitle:阿托伐他汀对小鼠压力负荷诱导的心室重构的保护作用及机制研究
- Author:
Di ZHAO
;
Wei WANG
;
Xiaojuan ZHANG
;
Weixing GUO
;
Tian ZHAO
;
Hongju JIANG
;
Zhuo ZHAO
- Publication Type:Journal Article
- Keywords:
Atorvastatin;
Pressure overload;
Transverse aortic constriction;
Myocardial hypertrophy;
inlfammatory factor
- From:
Chinese Circulation Journal
2015;(11):1090-1095
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the protective roll of atorvastatin on post-operative cardiac remodeling induced by transverse aortic constriction (TAC) in experimental mice with its possible mechanism.
Methods: A total of 48 C57BL/6 mice were randomly divided into 4 groups: Sham group, TAC group, TAC + valsartan group and TAC + atorvastatin group,n=12 in each group. Myocardial hypertrophy model was successfully established at 4 weeks after the operation, and then the animals were further treated by normal saline, valsartan 5mg/kg and atorvastatin 10mg/kg respectively for 8 weeks. Left ventricular anterior wall thickness at diastole (LVAWd), left ventricular posterior wall thickness at diastole (LVPWd), LVEF and left ventricular fractional shortening (FS) were examined by echocardiography, cardiac hypertrophy indexes were calculated. Protein expression of NF-κB was detected by Western blot analysis, cardiac tissue hydroxyproline (Hyp) level was measured by alkaline hydrolysis, serum levels of TNF-α, IL-1β were determined by ELISA, cardiac collagen deposition was identiifed by HE and Masson staining.
Results: Compared with Sham group, TAC group had increased LVAWd, LVPWd, cardiac hypertrophy indexes and increased area of cardiac fibrosis, allP<0.01; elevated protein expressions of NF-κB, Hyp, TNF-α, IL-1β, all P<0.01. Compared with TAC group, TAC + valsartan group and TAC + atorvastatin group presented improved cardiac hypertrophy indexes, decreased LVAWd, LVPWd and decreased area of cardiac ifbrosis, allP<0.01; reduced protein expressions of NF-κB, Hyp, TNF-α, IL-1β, allP<0.01.
Conclusion: Atorvastatin had protective roll on myocardial hypertrophy induced by pressure overload in experimental mice, which might be related to its anti-inlfammatory effect.
