RESEARCH ARTICLE Effects of β-sitosterol deriv m l N

is available at the end of the articleFibrosis is a wound healing process in which damaged regions are filled with an extracellular matrix (ECM). In liver, chronic injury leading to fibrosis occur in response to a variety of causes, including viral hepatitis, alcohol abuse, drugs, metabolic disease, autoimmune disease, or congenital abnormalities [1-4]. Liver damage provoke cellular changes that stimulate the recruitment of inflammatory cells and activate signal molecules that promote ECM accumulation [5]. Fibrogenic cell differentiation and ECM accumulation are usually induced by the transforming growth factor-beta (TGF-β) and the platelet-derived growth factor (PDGF) [5]. Induced liver fibrogenesis model have been studied with the TGF-β1 gene knock-out mice which showed accumulation of collagen-1 and alpha-smooth muscle actin (α-SMA) in their liver tissues [5,6]. Increased expression level of α-SMA is a marker of activated HSC model [5,7]. Hepatic stellate cells (HSCs), comprise 15 % of the total number of resident liver cells, adequate cellular model for investigation of liver fibrosis following thei