Involvement of Sirt1 in mouse myocardial hypertrophy induced by isorenin
XI Yu-hui1;MENG Qing-wei2;XU Chang-qing1;WANG Li-na1;LIN Yan3;LI Hong-zhu1;ZHANG Li1
1Department of Pathophysiology, 2The Third Clinical College, Harbin Medical University, Harbin 150081, China; 3Department of Pathophysiology, Qiqihaer Medical College, Qiqihaer 161006, China. E-mail: xucq45@126.com
Abstract:AIM: To investigate the expression and function of sirtuin 1 (Sirt1), one of the class III histone deacetylases, in hypertrophied mouse myocardium induced by isorenin (ISO). METHODS: The Kunming mice were randomly divided into 3 groups: control group, ISO group and ISO+nicotinamide (NAM) group. The myocardial hypertrophy was induced by dorsal subcutaneous injection of isorenin. Nicotinamide, an inhibitor against Sirt1, was given by peritoneal injection. Heart weight index (heart weight/body weight), hematoxylin and eosin staining, transmission electron microscope and mRNA expression of brain natriuretic peptide (BNP) were observed to identify the myocardial hypertrophy. The expression of Sirt1 in mRNA and protein levels was detected by RT-PCR and Western blotting, respectively. RESULTS: Compared to control group, the results of heart weight index, hematoxylin and eosin staining, the observation of transmission electron microscopy and mRNA expression of BNP showed that the mouse myocardial hypertrophy was induced by isorenin successfully. The Sirt1 expression was increased in hypertrophy model group (P<0.01 vs control group). Treatment with nicotinamide inhibited the cardiac hypertrophy induced by ISO (P<0.05 vs ISO group) and decreased the expression of Sirt1 (P<0.01 vs ISO group). CONCLUSION: Activation of Sirt1 might be involved in the process of myocardial hypertrophy stimulated by isorenin in mice.