期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 908, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.ejphar.2021.174354
关键词
Myocardial fibrosis; Forsythiaside B; alpha-SMA; Collagen III; TGF-beta 1/Smads pathway
资金
- National Natural Science Foundation of China [81673567, 82003701]
- Double First-Class University project [CPU2018GY34]
- Natural Science Research Projects in Colleges and Universities of Jiangsu Province [18KJB350002]
Forsythiaside B has been shown to protect myocardium from ischemia-reperfusion injury and inhibit myocardial fibrosis by suppressing the TGF-beta 1/Smad signaling pathway. It may be a rational therapeutic approach for the treatment of myocardial fibrosis.
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-beta 1, the expression of alpha-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-beta 1/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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据