Mechanistically, we found for the first time that Pue inhibited the overactivated NHE1 in HF, which may alleviate mitochondrial damage caused by calcium overload and improve HF by reducing the concentration of Na+ and Ca2+ ions; on the other hand, Pue inhibited the activation of the p38 pathway in HF, reduced the expression of TGF-β, and inhibited myocardial fibrosis. The gene discussed is TGFB1; the disease is hydrops fetalis.