Effect of curcumin on an animal model with hepatic fibrosis via tgf-β/smad signaling pathway

To study the protective effects and associated mechanisms of curcumin on hepatic fibrosis disease in rats. Thirty SD rats were randomly divided into three groups: a control group, a model group and a curcumin group. The control group was fed a normal diet, the model group was administered CCl4 in combination with a high fat diet to induce a hepatic fibrosis model, and the curcumin group followed the methods of the model group but was orally administered curcumin starting at 10 weeks. After 14 weeks, the effects of curcumin on lipid accumulation, hepatic fibrosis gene expression and Smad-3 activities were evaluated by biochemical analysis, HE-staining, quantitative real-time PCR and western blot.Curcumin treatment significantly alleviated the serum liver fibrosis index, hepatic steatosis, fibrosis and cell necrosis in CCl4-induced hepatic fibrosis rats. Moreover, curcumin reduced the mRNA levels of collagen I, α-SMA, and Smad3 as well as the levels of α-SMA and Smad3 proteins in the hepatic fibrosis livers. Curcumin was effective in preventing CCl4-induced increases in hepatic fibrosis. The effect was related to decreased lipid deposition, and it relieved liver fibrosis via inhibiting the TGF-β/Smad signaling pathway in the hepatic fibrosis livers.