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Effect of atorvastatin on cardiac function and HGF/c-Met signaling path-way after acute myocardial infarction in diabetic rats / 中国病理生理杂志
Article en Zh | WPRIM | ID: wpr-446062
Biblioteca responsable: WPRO
ABSTRACT
AIM:To investigate the effect of atorvastatin on myocardial apoptosis , ventricular remodeling and cardiac function after acute myocardial infarction (AMI) in diabetic rats, and to explore whether the effect is mediated by hepatocyte growth factor ( HGF)/c-Met signaling pathway .METHODS:Diabetes in 70 male SD rats was induced by in-traperitoneal injection of streptozotocin (STZ, 65 mg/kg).After 8 weeks, AMI was induced by the ligation of the left ante-rior descending coronary artery in the diabetic rats , and 32 surviving rats were divided into AMI group (n=16) and AMI+atorvastatin group ( n=16, 20 mg· kg -1 · d-1 ) at random.The similar surgical procedure was completed in sham group (n=11) without coronary ligation.Atorvastatin was given daily by gavage from the first day after AMI .Two weeks later, the cardiac function , pathological changes of myocardial tissues , myocardial apoptosis , and the expression of HGF and c-Met were compared among groups .RESULTS: AMI significantly reduced cardiac function , increased collagen volume fraction ( CVF) and myocardial apoptotic index , and up-regulated the expression of HGF and c-Met at mRNA and protein levels in AMI control group (P<0.05).The cardiac function was improved , and CVF and myocardial apoptotic index were reduced by the treatment with atorvastatin , which also up-regulated the expression of HGF and c-Met (P<0.05).CON-CLUSION:Atorvastatin significantly attenuates myocardial apoptosis and cardiac remodeling , and improves cardiac func-tion after AMI in diabetic rats by further enhancing the activation of HGF /c-Met pathway .
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Pathophysiology Año: 2014 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Pathophysiology Año: 2014 Tipo del documento: Article