Steatosis. 18 beta-glycyrrhetinic acid (18α-GL) can suppress the activation of hepatic stellate cells (HCSs) and induce their apoptosis by blocking the translocation of NF-kappaB into the nucleus, furthermore, it promoted the proliferation of hepatocytes in rats with CCl4-induced liver fibrosis [107] . GA inhibited type I collagen synthesis and progression of liver fibrosis probably through the suppression of collagen gene (COL1A2) promoter [108] . In transgenic mice expressing the HCV polyprotein fed an excess iron diet, SNMC prevented hepatic steatosis: this product attenuated ultrastructural alterations of mitochondria of the liver, activated mitochondrial β-oxidation with increased expression of carnitine palmitoyl transferase I and decreased the production of reactive oxygen species.