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American Journal of the Medical Sciences:
doi: 10.1097/MAJ.0b013e3181e2b353
Basic Investigation

Improved Cardiac Performance by Rosuvastatin Is Associated With Attenuations in Both Myocardial Tumor Necrosis Factor-[alpha] and p38 MAP Kinase Activity in Rats After Myocardial Infarction.

Xu, Yingying MD; Tang, Tingting MD, PhD; Ding, Yingjun MD, PhD; Yao, Rui MD, PhD; Xie, Jiangjiao MD, PhD; Liao, Mengyang MD; Xiao, Hong MD; Chen, Yong MD, PhD; Yu, Xian MD, PhD; Fu, Michael MD, PhD; Liao, Yuhua MD; Zhao, Guanghong MD, PhD; Cheng, Xiang MD, PhD

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Abstract

Introduction: Statins have been shown to exert anti-inflammatory effects. The aim of this study was to investigate whether rosuvastatin has favorable effect on ventricular remodeling after myocardial infarction (MI), whether this effect is associated with tumor necrosis factor (TNF)-α expression and p38 mitogen-activated protein (MAP) kinase pathway and, furthermore, whether there is close correlation between gene expression of TNF-α and activity of p38 MAP kinase.

Methods and Results: Adult male Wistar rats with acute MI were randomly divided into 2 groups: (1) rosuvastatin-treated group (MI-R) receiving rosuvastatin 20 mg/kg once daily, and (2) infarcted group (MI) receiving saline, when compared with sham-operated control group. Four weeks later, echocardiography, hemodynamics and Van Gieson staining were applied to evaluate left ventricular remodeling and cardiac function. Myocardial gene expression of TNF-α and activity of p38 MAP kinase were analyzed by real time-polymerase chain reaction and Western blot, respectively. The results demonstrated that increased TNF-α gene expression in noninfarcted areas was accompanied by activation of p38 MAP kinase pathway. Moreover, treatment of rosuvastatin markedly improved ventricular remodeling and cardiac function in rats, which was associated with attenuations in both TNF-α gene expression and p38 MAP kinase activity in myocardium without changes in serum lipid levels.

Conclusions: Treatment of rosuvastatin was able to improve cardiac remodeling and cardiac function after acute MI, which was associated with attenuations in both expression of TNF-α and activity of p38 MAP kinase in myocardium.

© Copyright 2010 Southern Society for Clinical Investigation

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