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

Eur J Pharmacol. 2021 Oct 5:908:174354. doi: 10.1016/j.ejphar.2021.174354. Epub 2021 Jul 17.

Abstract

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.

Keywords: Collagen III; Forsythiaside B; Myocardial fibrosis; TGF-β1/Smads pathway; α-SMA.

MeSH terms

  • Animals
  • Male
  • Mice
  • Transforming Growth Factor beta1*

Substances

  • TGFB1 protein, human
  • Transforming Growth Factor beta1