Effect of simvastatin on hyperlipidemia rat myocardial cells endoplasmic reticulum stress-related apoptosis.docVIP

 PAGE \* MERGEFORMAT 16 Effect of simvastatin on hyperlipidemia rat myocardial cells endoplasmic reticulum stress-related apoptosis Of: Qi Zhang Bin Zhou Ping Li method often Xiaodong Gan Hua Chen Mechanics [Abstract] Objective simvastatin in hyperlipidemic rat endoplasmic reticulum stress (ERS-related cardiac cell apoptosis and its mechanism. Methods Male Wistar rats of clean grade 24, were randomly divided into normal control group ( n = 8, normal diet feeding, hyperlipidemia group (n = 8, high fat diet feeding, the simvastatin group (n = 8, high fat diet + simvastatin 10 mg kg-1 d-1 irrigation gastric feeding .12 w, the fully automated serum biochemical analyzer triglyceride (TG) and cholesterol (TC) level, HE staining of the pathological changes of myocardial tissue, TUNEL assay Apoptosis, immunohistochemistry and RT PCR detection of signaling molecules ERS myocardial cells - glucose-regulated protein (GRP78 expression. Results Compared with normal control group, hyperlipidemia, serum levels of TG and TC, the degree of myocardial apoptosis and the expression levels of GRP78 were significantly rise higher (P lt;0.01 or P lt;0.05), and myocardial structural abnormalities, and hyperlipidemia group, the simvastatin group and the TC level of serum TG, myocardial apoptosis and GRP78 expression were significantly reduced but still higher than the control group (P lt;0.05) and myocardial structural abnormalities are improved. Conclusion hyperlipidemia way through the activation of cardiomyocyte apoptosis induced by ERS and lead to abnormal cardiac structure and simvastatin may suppress high fat way through the intervention ERS hyperlipidemia-induced myocardial apoptosis and reverse structural abnormalities in myocardial tissue, which play a cardioprotective effect. [Keywords:] rats, hyperlipidemia, endoplasmic reticulum stress, Apoptosis, simvastatin Effect of simvastatin on cardiomyocyte apoptosis induced by endoplasmic reticulum stress in rats with