Study On The Mechanism Of Protective Effect Of Tannic Acid On The Myocardial Hypertrophy Induced By Pressure Overload

Cardiac hypertrophy was a compensatory response to normal cardiac pressure overload, which eventually leads to heart failure. Therefore, the research of new drugs for the treatment of cardiac hypertrophy was one of the hotspots. In this paper, we explore the protective effect of tannic acid on myocardial hypertrophy and its potential mechanism. The rat model of cardiac hypertrophy was established by abdominal aortic banding. According to the random control principle, the rats treated with sham operation were used as the control group. Abdominal aortic banding rats were treated with tannic acid (20 and 40 mg/kg) or captopril and divided into low dose tannic acid group, high dose tannic acid group, and captopril group. The hemodynamic parameters of rats in each group were detected respectively, and then the related proteins and tissues were detected after the rats were killed. The results showed that the cardiac morphology and pathology of abdominal aortic banding rats treated with tannic acid were significantly improved, myocardial hypertrophy and apoptosis were decreased and the overexpression of Angiotensin II type 1 receptor and Angiotensin II type 2 receptor was decreased. In addition, the messenger Ribonucleic acid expression of extracellular signal regulated kinase 1/2, transforming growth factor-beta and matrix metalloproteinase-9 decreased. At the same time, tannic acid treatment decreased the activity and content of malondialdehyde and endothelin-1, and increased the content of superoxide dismutase, catalase, glutathione peroxidase, nitric oxide, and endothelial nitric oxide synthase. In addition, tannic acid down-regulated the expression of tumor necrosis factor-alpha, interleukin-1 beta, B-cell lymphoma-2 associated X protein and cysteine-dependent aspartate specific proteases-3 and up-regulated the expression of B-cell lymphoma-2. Tannic acid treatment can improve abdominal aortic banding induced cardiac hypertrophy effectively. Its cardioprotective effect is partly attributed to the reduction of myocardial oxidative stress, inhibition of inflammation, inhibition of fibrosis, reduction of apoptosis, increase of nitric oxide level, decrease of endothelin-1 level, and down-regulation of Angiotensin II type 1 receptor.