ArticleHistology and histopathology2022
Preclinical study of Shen Qi Li Xin formula in improving the development of chronic heart failure.
Article in Histology and histopathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Correlation between SUA and prognosis in CHF patients after revascularization.Journal of medical biochemistry · 2024Article
- Shengxian decoction protects against chronic heart failure in a rat model via energy regulation mechanisms.BMC complementary medicine and therapies · 2023Article
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Authors and funding
5 authors.
Funding
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 addition, 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.
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Registered trials
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