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Abstract

Resveratrol Inhibits Myocardial Apoptosis by Regulating the Protein Kinase R-like Endoplasmic Reticulum Kinase Endoplasmic Reticulum Stress Pathway and Improves Myocardial Remodeling and Cardiac Function after Myocardial Infarction

Author(s): C. Mei, Wenjing Liu and P. Sun*
Department of Cardiovascular Medicine, Hanyang Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430050, Hubei Province, 1Department of Internal Medicine, Hubei University Hospital, Wuhan 430000, Hubei Province, 2Department of Internal Medicine, Hubei University of Technology Hospital, Wuhan 430068, Hubei Province, China

Correspondence Address:
P. SUN, Department of Internal Medicine, Hubei University of Technology Hospital, Wuhan 430068, Hubei Province, China, E-mail: [email protected]


To analyze the effect of resveratrol on myocardial remodeling and cardiac function after myocardial infarction by inhibiting myocardial cell apoptosis through regulating silent information regulator 1/protein kinase R-like endoplasmic reticulum kinase pathway. 32 healthy male sprague dawley rats were divided into control group (without any treatment), model group (ligation of left anterior descending branch to establish a model), sham operation group (ligation of left anterior descending branch without ligation) and resveratrol group (ligation of left anterior descending branch+resveratrol 8 mg/kg/d), 8 rats each. The changes of cardiac function, myocardial remodeling, myocardial apoptosis and silent information regulator 1/protein kinase R-like endoplasmic reticulum kinase pathway related proteins were observed 4 w after modeling. Left ventricular end-diastolic diameter and left ventricular end-systolic dimension levels in the model group were significantly higher than those in the control group, left ventricular ejection fraction and left ventricular short axis shortening rate levels were significantly lower than those in the control group (p<0.01), left ventricular end-diastolic diameter and left ventricular end-systolic dimension levels in the resveratrol group were significantly lower than those in the model group and left ventricular ejection fraction and left ventricular short axis shortening rate levels were significantly higher than those in the model group (p<0.01). In the model group, the myocardial cells were arranged in a disordered manner and fibrogenic hyperplasia occurred, while the pathological changes of the myocardial cells in the resveratrol group were reduced compared with the model group. The collagen volume fraction of myocardial tissue in the model group was significantly higher than that in the control group (p<0.05) and the collagen volume fraction in the resveratrol group was significantly lower than that in the model group (p<0.05). The apoptosis rate of myocardial cells in the model group was significantly higher than that in the control group (p<0.01) and the apoptosis rate of myocardial cells in the resveratrol group was significantly lower than that in the model group (p<0.01). The expression levels of Phosphate-protein kinase R like endoplasmic reticulum kinase, Phosphate eukaryotic initiation factor 2 and Activating transcription factor 4 in the model group were significantly higher than those of the control group and the expression levels of Silent Information Regulator 1 were significantly lower than those of the control group (p<0.01). The expression levels of Phosphate-protein kinase R like endoplasmic reticulum kinase, Phosphate eukaryotic initiation factor 2 and Activating transcription factor 4 in the resveratrol group were significantly lower than those of the model group and the expression levels of silent information regulator 1 were significantly higher than those of the model group (p<0.01). Resveratrol can reduce apoptosis of myocardial cells after myocardial infarction by regulating the silent information regulator 1/protein kinase R-like endoplasmic reticulum kinase pathway endoplasmic reticulum stress pathway and improve myocardial remodeling and cardiac function in rats, providing a new target for clinical treatment of myocardial infarction.

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