ABSTRACT
Aim To study the effects of 2 ,3 ,4 ’ ,5-tet-rahydroxystilbene-2-O-β-D glucoside ( TSG ) on myo-cardial fibrosis ( MF) induced by isoproterenol ( ISO) in mice and its possible mechanism. Methods MF in mice was induced by subcutaneous injection of isoprot-erenol for 14 days. TSG (30,60,120 mg·kg-1 ) and captopril ( 40 mg · kg-1 ) were then administered by gavage to mice. The experiment was stopped 12 h after the last administration of the drugs. Hematoxylin-eosin ( HE) and Masson staining were used to estimate the extent of MF. Level of hydroxyproline in myocardial tissues was measured. Protein expressions of collagenⅠ, collagen Ⅲ and transforming growth factor-β1 (TGF-β1) in myocardial tissues were measured. Lev-els of superoxide dismutase ( SOD ) and glutathione peroxidase ( GSH-Px ) were determined. Results Compared with control mice, the level of hydroxypro-line in myocardial tissues was significantly increased in isoproterenol treated mice. Histological sections of iso-proterenol-treated hearts showed extensive myocardial fibrosis. And protein expressions of collagenⅠand col-lagen Ⅲwere markedly increased in isoproterenol trea-ted mice. However, therapy with TSG decreased the level of hydroxyproline in myocardial tissues, ameliora-ted the degree of myocardial fibrosis, and reduced the collagen expressions induced by isoproterenol adminis-tration. Moreover, treatment with TSG decreased TGF-β1 protein expression and elevated the myocardial SOD and GSH-Px activity. Conclusion TSG can inhibit MF formation induced by ISO in mice which might be due to regulating TGF-β1 protein expression and its an-tioxidant effect.