Resveratrol attenuates the progress of liver fibrosis via the Akt/nuclear factor-κB pathways

Liver fibrosis is a wound-healing response to chronic liver injury that results in the accumulation of extracellular matrix proteins. It eventually leads to cirrhosis of the liver and liver failure, and it is a critical threat to the health and lives of patients with chronic liver diseases. No effective treatment is currently available. Resveratrol is a polyphenol with antioxidant, anti-cancer and anti-inflammatory properties. It has been reported that resveratrol prevents liver fibrosis, possibly by inhibiting NF-kappa B activation. The present study investigated the mechanisms by which resveratrol prevented liver fibrosis, focusing on the possible involvement of the NF-kappa B pathway. Mice with carbon tetrachloride (CCl4)-induced liver fibrosis were treated with various concentrations of resveratrol. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor (TNF)-alpha were detected by ELISAs. Expression of a-smooth muscle actin (alpha-SMA), collagen I, inhibitor of NF-kappa B (I kappa B) and NF-kappa B were detected by western blot analysis. In addition, the present study examined the effects of resveratrol on the expression of fibrosis markers in LX-2 cells. Western blot analysis was further used to detect the levels of Akt and phosphorylated Akt, as well as the nuclear levels of I kappa B, phosphorylated I kappa B and NF-kappa B p65. The expression of alpha-SMA in resveratrol-treated LX-2 cells was detected by immunofluorescence and flow cytometry, which demonstrated that resveratrol decreased the expression of alpha-SMA in LX-2 cells. Resveratrol also decreased CCl4-induced upregulation of serum AST, ALT, TNF-alpha, alpha-SMA and collagen I. Finally, resveratrol prevented the activation of NF-kappa B and Akt. The results of the present study therefore indicated that resveratrol attenuates liver fibrosis via the Akt/NF-kappa B pathways.