| Abstrakt: |
Background: The aim of this study is to investigate the mechanism of action underlying the therapeutic effects of the national patent Chinese medicine compound "Qiangxinhuoli prescription (QXHLF)" on chronic heart failure (CHF). Methods: In vitro, the H9C2 cell model was induced by ANGII, and cell proliferation and related protein expression were detected by Cell Counting Kit-8 and Western blot. In vivo, A rat model of CHF was prepared by ligation of the left anterior descending coronary artery. The effects of QXHLF on cardiac function in CHF rats were evaluated by cardiac index, hemodynamic changes, enzyme-linked immunosorbent assay, hematoxylin-eosin staining, immunohistochemistry, Western blot and RT-PCR. The expression of pro-apoptotic factors and anti-apoptotic factors, as well as TGFβ1, p-p38, TAK1 mRNA, and protein, were detected. Results: In vitro, QXHLF has a significant inhibitory effect on the proliferation of H9C2 cells. QXHLF can reduce the expression levels of TAK1, TGFβ1, p-p38, Caspase3 and BAX proteins in H9C2 cells, and increase the expression level of BCL2 protein. In vivo, QXHLF has the potential to increase left ventricular systolic pressure, maximum rate of change in left ventricular pressure while decreasing left ventricular end diastolic pressure, and inhibiting the serum levels of brain natriuretic peptide. Moreover, QXHLF exhibits significant improvements in the pathological alterations of myocardial cells and fibers in CHF rats, leading to enhanced myocardial tissue morphology and notable advantages in combating myocardial fibrosis. QXHLF can reduce the levels of BAX and Caspase3 and up-regulate the expression of BCL2, thereby inhibiting cardiomyocyte apoptosis. Furthermore, QXHLF demonstrates inhibitory effects on the mRNA and protein expression levels of TGFβ1, TAK1, and p-p38 in the heart tissue of the CHF rat model. Conclusion: These findings indicate that QXHLF has a therapeutic effect on CHF by inhibiting the p38-MAPK signaling pathway, reducing myocardial fibrosis, preventing apoptosis, inhibiting cell proliferation, and restoring myocardial injury. [ABSTRACT FROM AUTHOR] |
