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

Jing Sun, Jiaxin Zhu, Lei Chen, Bingjing Duan, Ruyi Wang, Mengyuan Zhang, Jian Xu, Wenyuan Liu, Yunhui Xu, Feng Feng, Wei Qu

European journal of pharmacology 2021 Oct 05

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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