[Protection of vasodilatory function in rats with post-infarction heart failure by salvianolic acid B via modulating Piezo1 channel].

To explore the regulation of vasodilatory function in rats with post-infarction heart failure by salvianolic acid B(Sal-B) based on the mechanosensitive ion channel, namely Piezo1. A post-infarction heart failure model of rats was prepared by ligation of the left anterior descending coronary artery. After successful modeling, the rats were randomly divided into the model group, Sal-B group(0.5 g·kg~(-1)), and sham-operated group, and they were gavaged for 14 days, once a day. At the end of the experiment, echocardiography was used to detect cardiac function indexes such as LVEF, LVFS, SV, and CO in rats; biochemical analysis was used to detect serum CK, CK-MB, and LHD activities; ELISA was used to detect serum ANP, BNP, and AngⅡ contents; TTC staining was used to observe the myocardial infarction area, and the thoracic aorta was taken to perform an ex vivo vascular ring test, so as to determine endothelium-dependent dilation(EDD) and endothelium-independent dilation(EID) of different groups. The effects of Piezo1 channel agonist(Yoda1) and inhibitor(Dooku1) on EDD and EID were detected; Masson staining was performed to observe the structural changes of the thoracic aorta; immunofluorescence staining was performed to detect the protein expression of Piezo1 and CD31 in the thora-cic aorta of the rats, and Western blot was performed to detect the expression level of Piezo1 in the vessel. The results showed that compared with those of the model group, the LVEF, LVFS, CO, and SV of the Sal-B group were significantly increased, and the myocardial infarction area was reduced. The activities of serum CK, CK-MB, and LDH were decreased, and the levels of ANP, BNP, and AngⅡ were down-regulated. The EDD and EID of the thoracic aorta were improved, and the expression of Piezo1 in the vascular endothelial cells of the rats with post-infarction heart failure was increased to enhance the responsiveness of Yoda1 to EDD, and the Piezo1 expression in vascular smooth muscle cells was up-regulated to increase the responsiveness of Dooku1 to EID. In conclusion, Sal-B can improve cardiac function and protect vasodilatory function in rats with post-infarction heart failure, and its effect may be related to the expression of Piezo1 in vascular endothelial cells and smooth muscle cells.