Title: Effect of simvastatin on cardiomyocyte apoptosis induced by endoplasmic reticulum stress in rats with hyperlipidemia
Abstract: Objective To investigate the cardioprotection and its mechanism of simvastatin on cardiomyocyte apoptosis induced by endoplasmic reticulum stress in rats with hyperlipidemia.Methods Twenty-four male wistar rats were randomly divided into three groups:normal control group (n=8,fed with normal diet),high fat group (n=8,fed!with high fat diet ) and simvastatin group(n=8,fed with high fat diet and received simvastatin 10mg·kg-1·d-1 by gastric irrigation).After twelve weaks,the serum triglycerides (TG) and cholesterol (TC) levels were determined by completely automatic biochemistry meter.The pathological changes of myocardial tissue were detected by HE staining.The apoptotic cardiomyocytes of myocardial tissue were tested by TUNEL.The expression of endoplasmic reticulum stress (ERS) associated molecle-glucose regulated protein (GRP) 78 in myocardial tissue was investigated by immunohistochemistry and RT-PCR.Results Compared with normal control group,the serum TG and TC levels,and the numbers of apoptotic cardiomyocytes as well as the expression of GRP78 protein and GRP78 mRNA in myocardial tissue were significantly increased in high fat group (P0.01 or 0.05).Compared with the high fat group,the serum TG and TC levels,and the numbers of apoptotic cardiomyocytes as well as the expression of GRP78 protein and GRP78 mRNA in myocardial tissue were remarkably reduced in simvastatin group but still higher than those in normal control group (all P0.05).Conclusions The hyperlipidemia can induce myocardiocyte apoptosis through activating ERS signaling pathways.The simvastatin can inhibit the myocardocyet apoptosis induced by hyperlipidemia through amelioration of ERS.
Publication Year: 2010
Publication Date: 2010-01-01
Language: en
Type: article
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