Pharmacodynamics and mechanism of Astragali radix and Anemarrhenae rhizoma in treating chronic heart failure by inhibiting complement activation.

Astragali radix (AR) and Anemarrhenae rhizoma (AAR) are used clinically in Chinese medicine for the treatment of chronic heart failure (CHF), but the exact therapeutic mechanism is unclear. In this study, a total of sixty male C57BL/6 mice were split into six groups at Sham, Model, AR, AAR and AR-AAR. The Sham group mice were only opened the chest without ligation. The other groups mice were opened the chest and ligated the transverse aortic to construct the transverse aortic constriction (TAC) model. After eight weeks of feeding, they were given medicines by gavage for four weeks. Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were detected by echocardiography. Heart weight index (HWI) and wheat germ agglutinin (WGA) staining were used to evaluate cardiac hypertrophy. Hematoxylin-eosin (HE) staining was used to observe the pathological morphology of myocardial tissue. Masson staining was used to evaluate myocardial fibrosis. The content of serum brain natriuretic peptide (BNP) was detected by ELISA kit. The content of serum immunoglobulin G (IgG) was detected by immunoturbidimetry. The mechanism of AR-AAR in the treatment of CHF was explored by proteomics. Western blot was used to detect the protein expressions of complement component 1s (C1s), complement component 9 (C9) and terminal complement complex 5b-9 (C5b-9). The results show that AR-AAR inhibits the expression of complement proteins C1s, C9 and C5b-9 by inhibiting the production of IgG antibodies from B cell activation, which further inhibits complement activation, attenuates myocardial fibrosis, reduces HWI and cardiomyocyte cross-sectional area, improves cardiomyocyte injury, reduces serum BNP release, elevates LVEF and LVFS, improves cardiac function and exerts myocardial protection.