Key result
Shengmaiyin improves cardiac function and reduces myocardial fibrosis in rats with induced hypertrophy.
Why the study?
Shengmaiyin has clear effects in treating and preventing cardiac hypertrophy, but the underlying mechanisms remain unclear.
Does Shengmaiyin (SMY) improve cardiac hypertrophy in isoproterenol (ISO)-induced myocardial hypertrophy in rats?
Does Shengmaiyin (SMY) improve cardiac hypertrophy in isoproterenol (ISO)-induced myocardial hypertrophy in rats?
Answers are grounded in this paper and cite their sources.
Shengmaiyin ameliorates isoproterenol-induced myocardial hypertrophy in rats by improving cardiac function, regulating intestinal flora, and inhibiting the HIF1α/PPAR signalling pathway.
Background. The gut-cardiac axis theory provides new insights into the complex mechanisms of cardiac hypertrophy and provides new therapeutic targets. Cardiac hypertrophy is a risk factor for heart failure. Shengmaiyin (SMY) is a traditional Chinese medicine formula with clear effects in the treatment and prevention of cardiac hypertrophy, but the mechanism by which it improves cardiac hypertrophy is still unclear. Therefore, this study aimed to investigate the protective effect and mechanism of SMY on isoproterenol (ISO)-induced myocardial hypertrophy in rats. Methods. First, various pharmacodynamic methods were used to evaluate the therapeutic effect of SMY on ISO-induced myocardial hypertrophy in rats. Then, 16S rDNA amplicon sequencing technology was used to study the effect of SMY on the intestinal flora of rats with myocardial hypertrophy. Finally, the mechanism underlying the effect of SMY on cardiac hypertrophy was predicted by bioinformatics network analysis and verified by Western blotting. Results. SMY increased ejection fraction (EF%) and left ventricular fractional shortening (FS%), ameliorated myocardial cell injury and fibrosis, regulated blood lipids and energy metabolism, and decreased cardiac hypertrophy marker gene expression. The gut microbiota of ISO-induced myocardial hypertrophy rats were significantly changed, while SMY effectively ameliorated the dysbiosis of the intestinal flora in rats with myocardial hypertrophy, especially Prevotella 9, Lactobacillus, and Clostridium. Mechanistic studies have shown that the anticardiac hypertrophy effect of SMY is related to the inhibition of the expression of HIF1α/PPAR signalling pathway-related proteins. Conclusion. SMY significantly improves cardiac function, relieves myocardial cell fibrosis and necrosis, resists cardiac hypertrophy, improves blood lipid metabolism and energy metabolism, regulates intestinal microbial disturbance, and protects the heart.
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Ming et al. (2022) studied Isoproterenol (ISO)-induced myocardial hypertrophy. Shengmaiyin (SMY) vs. Control (ISO-induced myocardial hypertrophy without SMY) was evaluated on Cardiac function (EF%, FS%), myocardial cell injury and fibrosis, and intestinal flora dysbiosis. Shengmaiyin (SMY) improved cardiac function, relieved myocardial fibrosis, and ameliorated intestinal flora dysbiosis in rats with isoproterenol-induced myocardial hypertrophy.
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