Chlorella vulgaris supplementation attenuates the progression of liver fibrosis through targeting TGF-β-signaling pathway in the CCl4-induced liver fibrosis in rats

Abstract

The purpose of this study is to investigate the molecular mechanism underlying hepatoprotective effect of Chlorella vulgaris extract (CVE). The administration of both doses of CVE attenuated liver damage and decreased serum markers and oxidative stress parameters dramatically. Also, CVE treatment downregulated hepatic gene expression of collagen type1 (Col1a1), fibronectin (Fn1), transforming growth factor-beta 1 (Tgfb1), transforming growth factor-beta receptor 2 (Tgfbr2) and SMAD family member 3 (Smad3) significantly. Hepatic level of TGF-β1 protein was decreased by CVE treatment significantly. CVE supplementation restraints liver fibrosis progression through amelioration of oxidative stress status and targeting TGF-β signaling pathway.