1. Salvanic acid B inhibits myocardial fibrosis through regulating TGF-β1/Smad signaling pathway.
- Author
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Gao, Hongyan, Bo, Zhe, Wang, Qin, Luo, Ling, Zhu, Haiyi, and Ren, Yi
- Abstract
Abstract 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-β), 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-β1 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-β1 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-β/Smads signaling pathway, including TGF-β1, 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-β/Smads signal transduction pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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