Salvanic acid B inhibits myocardial fibrosis through regulating TGF-β1/Smad signaling pathway.

Objective: Salvanic Acid B (Sal B) was proved to show significant effect against fibrosis and myocardial injury. This study aimed to investigate the protective effects and the mechanisms of Sal B on myocardial fibrosis. Methods: The mice were randomly assigned to five groups: control group, model group, positive group, low-dose group, high-dose group. Hematoxylin-Eosin (HE) staining and Masson staining were used to assess the myocardial physiological changes and measure the myocardial fibrosis area. Expression of transforming growth factor-beta (TGF-beta), drosophila mothers against decapentaplegic (Smad)2, Smad3 and Smad7 were analyzed by immunohistochemistry and real-time PCR. On the other hand, mouse cardiac fibroblasts (CFs) cells were co- treated with 20 ng/mL TGF-beta 1 and different concentrations of Sal B (5, 10, and 20 ng/mL) for 24 h. The cells morphology changes were assessed under a microscope, and the protein expressions induced by TGF-beta 1 were detected by Western blot. Results: Compared with the model group, myocardial collagen fibers decreased obviously with Sal B treatment (p < 0.05). Moreover, the expression of key signal molecules of the TGF-beta/Smads signaling pathway, including TGF-beta 1, Smad2 and Smad3 proteins decreased, while the expression of Smad7 increased in Sal B treatment groups as compared to those of the model group (p < 0.05). On the other hand, results of CFs studies were also consistent with those animals. Conclusions: Sal B could inhibit the myocardial fibrosis process through regulating TGF-beta/Smads signal transduction pathways.