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Abstract

Effect of Simvastatin on Ventricular Remodeling in Rats with Acute Myocardial Infarction through Transforming Growth Factor-Beta/SMAD Signaling Pathway

Author(s): Yunfang Wang, Bo Wu, Luping Yuan and Liang Zhang*
Department of Internal Medicine, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province 310012, 1Department of Cardiovascular Medicine, The First Teaching Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 16369, China

Correspondence Address:
Liang Zhang, Department of Cardiovascular Medicine, The First Teaching Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 16369, China, E-mail: zhangliang853@163.com


To investigate the effect of simvastatin on ventricular remodeling in rats with acute myocardial infarction through the transforming growth factor beta/SMAD signaling pathway. A rat acute myocardial infarction model was established by ligating the left anterior descending coronary artery as the acute myocardial infarction group; treated with low, medium and high doses (10 mg/kg, 20 mg/kg and 40 mg/kg) of simvastatin as acute myocardial infarction+simvastatin-low, acute myocardial infarction+simvastatin-medium, acute myocardial infarction+simvastatin-high groups. Set up another sham operation group (sham group). 4 w later, the rats' body weight, hemodynamic acute myocardial infarction indicators, and blood lipid levels were detected; quantitative reverse transcription polymerase chain reaction and Western blot were used to detect the expression of transforming growth factor beta 1, SMAD2/3 messenger ribonucleic acid and protein. Compared with the sham group, the left ventricular weight and left ventricular weight index of the rats were significantly increased (p<0.05); compared with the acute myocardial infarction group, simvastatin significantly reduced the left ventricular weight and left ventricular weight index of the rats (p<0.05). Compared with the sham group, the left ventricular systolic pressure of the acute myocardial infarction group was significantly increased, and the left ventricular end-diastolic pressure, +dp/dtmax and -dp/dtmax were significantly decreased (p<0.05); compared with the acute myocardial infarction group, simvastatin significantly reduced the rat left ventricular end-diastolic pressure, significantly increased left ventricular end-diastolic pressure, +dp/dtmax and -dp/dtmax (p<0.05). Compared with the sham group, the expression of transforming growth factor beta 1, SMAD2, SMAD3 messenger ribonucleic acid and protein in the acute myocardial infarction group was significantly increased (p<0.05); compared with the acute myocardial infarction group, simvastatin significantly reduced the expression of transforming growth factor beta 1, SMAD2, SMAD3 messenger ribonucleic acid and protein in the rat (p>0.05). Simvastatin can alleviate ventricular remodeling in acute myocardial infarction rats by inhibiting the transforming growth factor beta/SMAD signaling pathway.

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