Preclinical study of Shen Qi Li Xin formula in improving the development of chronic heart failure

xlomafota13 shared this article with you from Inoreader Preclinical study of Shen Qi Li Xin formula in improving the development of chronic heart failure Via Cellular and Molecular Biology Histol Histopathol. 2022 Mar 25:18454. doi: 10.14670/HH-18-454. Online ahead of print. ABSTRACT Chronic heart failure (CHF) is a common clinical heart disease. In recent years, traditional Chinese medicines have shown good outcomes in CHF treatment. We aimed to explore the therapeutic effect of Shen Qi Li Xin formula (SQLXF) in CHF. CHF rats were treated with SQLXF at the doses of 8.48, 16.96, and 33.92 g/kg/d once a day for 4 weeks by intragastric administration. The hemodynamic and cardiac function parameters of the rats were monitored by conduction echocardiography. In our results, SQLXF treatment at the doses of 16.96 and 33.92 g/kg/d significantly improved the haemodynamics and cardiac function of CHF rats by enhancing the levels of LVSP, +dp/dtmax, -dp/dtmax, LVEF and LVFS and reducing the levels of LVEDP, LVEDD and LVESD. SQLXF treatment at 16.96 and 33.92 g/kg/d also attenuated the damage of myocardial tissues in CHF rats. In a ddition, compared with normal rats, the number of pericytes was reduced in myocardial tissues of CHF rats. SQLXF treatment at the doses of 16.96 and 33.92 g/kg/d obviously increased the number of pericytes and proliferation of endothelial cells and promoted angiogenesis in myocardial tissues of CHF rats. In vitro, SQLXF impaired low-oxygen-induced inhibition of cell viability and promotion of apoptosis in primary pericytes. Importantly, SQLXF enhanced the adhesion ability of pericytes to endothelial cells. In conclusion, SQLXF improved myocardial injury in CHF rats by enhancing the interaction between pericytes and endothelial cells, suggesting that SQLXF may be a potential drug for CHF treatment. PMID:35333374 | DOI:10.14670/HH-18-454 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.