Hongyan Gao1, Zhe Bo2, Qin Wang3, Ling Luo2, Haiyi Zhu2, Yi Ren4. 1. Chongqing Key Laboratory of Traditional Chinese Medicine to Prevent and Treat Autoimmune Diseases, Chongqing Hospital of Traditional Chinese Medicine, Chongqing 400021, PR China. 2. Department of Cardiology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing 400021, PR China. 3. Department of Pharmacy, Chongqing Hospital of Traditional Chinese Medicine, Chongqing 400021, PR China. 4. Department of Cardiology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing 400021, PR China. Electronic address: yiren827722@163.com.
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.
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), drosophilamothers 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.