Abstract: This study was focus on investigating the anti-liver fibrosis effects of insulin-like growth factor-1(IGF-1) in vitro. The effects of IGF-1 on human liver L-02 cell viability and cell cycle were observed. CCl₄-induced L-02 cell injury was set up to detect the anti-apoptotic activity of insulin-like growth factor-1(IGF-1). Transforming growth factor β1(TGF-β1)induced hepatic stellate cell line(HSC-T6)were used as a liver fibrosis model in vitro to analyze the effects of IGF-1 on the expression of liver fibrosis proteins and intracellular TGF-β1/Smad signaling pathway in HSC-T6 cells. The results showed that IGF-1 could relieve the growth inhibition effects of TGF-β1 on L-02 cells, increase the viability of L-02 cells injured by CCl₄, decrease the expression of liver fibrosis proteins, and inhibit the TGF-β1/Smad signaling pathway by inhibiting the phosphorylation of Smad3. Our study suggested that IGF-1 exerted anti-liver fibrosis effects by stimulating L-02 cells proliferation, reducing cell damage and inhibiting ECM accumulation via interfering TGF-β1/Smad signaling pathway.