Forsythiaside B inhibits myocardial fibrosis via down regulating TGF-β1/Smad signaling pathway.

Forsythiaside B is the major ingredient of Callicarpa kwangtungensis Chun, and has been proven to protect myocardium from ischemia-reperfusion injury to achieve myocardial protection. However, the effect of forsythiaside B on adverse myocardial fibrosis remains unclear. In the present study, the myocardial fibrosis animal models were established induced by isoproterenol (ISO) to investigate whether forsythiaside B exhibited antifibrotic actions. Forsythiaside B was found to significantly improve the cardiac ejection fraction and fractional shortening rate of myocardial fibrosis mice compared with the normal saline group. In addition, forsythiaside B could lower the level of TGF-β1, the expression of α-SMA and collagen III. Forsythiaside B down-regulated the expression of Smad4 and the phosphorylation level of Smad3, which indicates that forsythiaside B could suppress myocardial fibrosis by inhibiting the TGF-β1/Smad signaling pathway. These results demonstrated that forsythiaside B could prevent myocardial fibrosis in ISO-induced mice, and may be a potentially rational therapeutic approach for the treatment of myocardial fibrosis. Copyright © 2021 Elsevier B.V. All rights reserved.

Citation

Jing Sun, Jiaxin Zhu, Lei Chen, Bingjing Duan, Ruyi Wang, Mengyuan Zhang, Jian Xu, Wenyuan Liu, Yunhui Xu, Feng Feng, Wei Qu. Forsythiaside B inhibits myocardial fibrosis via down regulating TGF-β1/Smad signaling pathway. European journal of pharmacology. 2021 Oct 05;908:174354

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PMID: 34284013

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