AIM: To investigate the correlation between the antifibrotic effect of baicalin and serum cytokine production in rat hepatic fibrosis. METHODS: Forty male Sprague-Dawley rats were divided randomly into four groups: normal control group, model group, baicalin-treated group, and colchicine-treated group. Except for the normal control group, all rats in the other groups were administered with carbon tetrachloride to induce hepatic fibrosis. At the same time, the last two groups were also treated with baicalin or colchicine. At the end of the 8 wk, all animals were sacrif iced. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10 were measured. Liver index, hepatic hydroxyproline content and the degree of liver fibrosis were also evaluated. RESULTS: The levels of ALT, AST and liver index in the baicalin-treated group were markedly lower than those in the model group (ALT: 143.88 ± 14.55 U/L vs 193.58 ± 24.35 U/L; AST: 263.66 ± 44.23 U/L vs 404.37 ± 68.29 U/L; liver index: 0.033 ± 0.005 vs 0.049 ± 0.009, P < 0.01). Baicalin therapy also significantly attenuated the degree of hepatic fibrosis, collagen area and collagen area percentage in liver tissue (P < 0.01). Furthermore, the levels of serum TGFβ1, TNF-α and IL-6 were strikingly reduced in the baicalin-treated group compared with the model group, while the production of IL-10 was up-regulated: (TGF-β1: 260.21 ± 31.01 pg/mL vs 375.49 ± 57.47 pg/mL; TNF-α: 193.40 ± 15.18 pg/mL vs 260.04 ± 37.70 pg/mL; IL-6: 339.87 ± 72.95 pg/mL vs 606.47 ± 130.73 pg/mL; IL-10: 506.22 ± 112.07 pg/mL vs 316.95 ± 62.74 pg/mL, P < 0.01). CONCLUSION: Baicalin shows certain therapeutic effects on hepatic fibrosis, probably by immunoregulating the imbalance between prof ibrotic and antif ibrotic cytokines. To investigate the correlation between the antifibrotic effect of baicalin and serum cytokine production in rat hepatic fibrosis. METHODS: Forty male Sprague-Dawley rats were divided randomly into four groups: normal control group, model group, baicalin-treated group, and colchicine -treated group. Except for the normal control group, all rats in the other groups were administered with carbon tetrachloride to induce hepatic fibrosis. At the same time, the last two groups were also treated with baicalin or colchicine. At the end of the 8 Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), transforming growth factor (TGF) -β1, tumor necrosis factor (TNF) -α, interleukin (IL) -6 and IL-10 were measured. Liver index, hepatic hydroxyproline content and the degree of liver fibrosis were also evaluated. RESULTS: The levels of ALT, AST and liver index in the baicalin-treated group were markedly lower than those in the model group (ALT: 1 43.88 ± 14.55 U / L vs 193.58 ± 24.35 U / L; AST: 263.66 ± 44.23 U / L vs 404.37 ± 68.29 U / L; liver index: 0.033 ± 0.005 vs 0.049 ± 0.009, P <0.01) The levels of serum TGFβ1, TNF-α and IL-6 were strikingly reduced in the baicalin-treated group compared with the model (P <0.01). group: while the production of IL-10 was up-regulated: (TGF-β1: 260.21 ± 31.01 pg / mL vs 375.49 ± 57.47 pg / mL; TNF- α: 193.40 ± 15.18 pg / mL vs 260.04 ± 37.70 pg / mL ; IL-6: 339.87 ± 72.95 pg / mL vs. 606.47 ± 130.73 pg / mL; IL-10: 506.22 ± 112.07 pg / mL vs. 316.95 ± 62.74 pg / mL, P <0.01). CONCLUSION: Baicalin shows certain therapeutic effects on hepatic fibrosis, probably by immunoregulating the imbalance between prof ibrotic and antif ibrotic cytokines.