Effect of Qishen Yiqi Dropping Pill on Intervention of Vascular Endothelial Function in Rats with Acute Myocardial Infarction

  • Xiaohuan Wang
Keywords: Qishenyiqi dropping pill; Acute myocardial infarction; Protein expression; Vascular endothelial function


Acute myocardial infarction is a serious threat to human health and life. With the advancement of coronary revascularization, the mortality rate of patients has decreased significantly, but the incidence of heart failure has increased significantly. In this paper, the effects of Qishen Yiqi Dropping Pill on vascular endothelial function in rats with acute myocardial infarction were observed, and the mechanism of action was explored based on the expression of TGF-β1/Smads pathway. After 4 weeks of intervention, HE and Masson staining were performed on the rat heart, and the myocardial collagen volume fraction was calculated. Real-time quantitative PCR and Western blot were used to detect the expression of TGF-β1, Smad2 and Smad7 mRNA and protein in cardiac tissue. The results showed that HE staining showed that a large area of connective tissue was formed in the wall of the model group, the wall of the chamber was significantly thinner, and the myocardial cells were obviously edematous and a large number of inflammatory cells infiltrated. In each treatment group, the area of connective tissue in the wall was reduced, and cell edema and inflammatory cells were alleviated. Masson staining showed myocardial fibrosis in each group of rats after modeling. Compared with the model group, CVF was significantly lower in each treatment group (P<0.01). Compared with the sham operation group, the expression of TGF-β1 and Smad2 mRNA and protein in the model group increased significantly, and Smad7 decreased significantly. Compared with the model group, the expression of TGF-β1 and Smad2 mRNA and protein in QSYQ-H and captopril were down-regulated, and Smad7 expression was down-regulated. Up-regulated (P<0.05). Qishen Yiqi Dropping Pill can inhibit myocardial fibrosis after myocardial infarction in rats, and its mechanism may be related to the regulation of gene and protein expression of TGF-β1/Smads pathway-related factors.