Huangqi Shengmai Yin ameliorated isoprenaline-induced myocardial fibrosis and improved cardiac function in rats by activating Sirtuin 3 and inhibiting the TGF-β/Smad signaling pathway.
Does Huangqi Shengmai Yin ameliorate myocardial fibrosis and cardiac dysfunction in rats with isoprenaline-induced myocardial fibrosis?
In a rat model of isoprenaline-induced myocardial fibrosis, Huangqi Shengmai Yin improved cardiac function and reduced fibrosis via Sirt3 activation and TGF-β/Smad pathway inhibition.
Myocardial fibrosis (MF) is an important pathological process in which a variety of cardiovascular diseases transform into heart failure. The main manifestation of MF is the excessive deposition of collagen in the myocardium. Here, we explored whether Huangqi Shengmai Yin (HSY) can inhibit isoprenaline (ISO)-induced myocardial collagen deposition in rats, thereby reducing the cardiac dysfunction caused by MF. The results of echocardiography showed that HSY upregulated fractional shortening and ejection fraction, and reduced the left ventricular systolic dysfunction in the rats with MF. Pathological results showed that HSY protected myocardium, inhibited apoptosis, and effectively reduced collagen deposition. HSY also inhibited the expression of collagen I and III and α-smooth muscle actin (α-SMA) in the heart tissue. HSY increased the expression of Sirtuin 3 (Sirt3) and inhibited the protein levels of the components in the transforming growth factor-β (TGF-β)/Smad pathway. At the same time, it also regulated the expression of related proteins in the matrix metalloproteinases family. In summary, HSY played a therapeutic role in rats with ISO-induced MF by protecting myocardium and inhibiting collagen deposition. Therefore, HSY is a potential therapeutic agent for ameliorating MF.
Pan et al. (Fri,) conducted a other in Myocardial Fibrosis (n=50). Huangqi Shengmai Yin (HSY) vs. Isoprenaline (ISO) alone and Captopril was evaluated on Cardiac function (Ejection Fraction and Fractional Shortening) and collagen deposition. Huangqi Shengmai Yin ameliorated isoprenaline-induced myocardial fibrosis and improved cardiac function in rats by activating Sirtuin 3 and inhibiting the TGF-β/Smad signaling pathway.