摘要
AIM： To study the effect of interleukin-10 （IL-10） on the expression of transforming growth factor β1 （TGF-β1） in hepatic fibrosis rats and the anti-fibrotic role of exogenous IL-10. METHODS： Hepatic fibrosis was induced by carbon tetrachloride administered （CCh） intraperitoneally. The experiment was performed in two stages. In the first stage, 60 SD rats were divided randomly into normal control group I（GNI, n = 8）, hepatic fibrosis group（GC, n = 28）and IL-10 intervened group（GI, n = 24）. At the beginning of the 7^th and 11^th wk, hepatic stellate cells （HSCs） were isolated, reverse transcription-polymerase chain reation （RT-PCR） and immunocytochemistry were performed to detect the expression of TGF-β1 in HSCs. Histological examination was used to determine the degree of hepatic fibrosis. In the second stage, 47 SD rats were divided randomly into normal control group 2 （GN2, n = 6）and CCh group（GZ, n = 41）. At the end of the 9th week, rats in GZ group were allocated randomly into model group（GM, n = 9）, IL-10 treatment group（GT, n = 9） and recovered group （GR, n = 9）. At the end of the 12^th week, all rats were sacrificed. RT-PCR and immuno- histochemistry were performed to detect the expression of TGF-β1 in liver tissue. ELISA was used to assay serum TGF-β1 levels. RESULTS： Hepatic fibrosis developed in rats with the increase of the injection frequency of CCI4. In the first stage, hepatic fibrosis developed and HSCs were isolated successfully. At the 7^th and 11^th week, TGF-β1 mRNA in GC group increased significantly compared with that in GN1（P = 0.001/0.042） and GI groups（P = 0.001/0.007）, whereas there was no significant difference between the two groups. The levels of TGF-β1 at the beginning of the 7^th wk was higher than that of the 11^th wk （P = 0.049）.Immunocytochemistry results of TGF-β1 were consistent with the above findings. In the second stage, TGF-β1 increased significantly in GM group compared to GN2. Alter treatment with IL-10, TGF-β1 declined obviously. The expression of TGF-β1 decreased in GR group but was still higher than that in GT group. CONCLUSION： The levels of TGF-β1 are increased in hepatic fibrosis rats and decreased alter treatment with exogenous IL-10. IL-10 may play an anti-fibrotic role by suppressing TGF-β1 expression.
AIM: To study the effect of interleukin-10 (IL-10) on the expression of transforming growth factorβ1 (TGF-β1) in hepatic fibrosis rats and the anti-fibrotic role of exogenous IL-10. METHODS: Hepatic fibrosis was induced by carbon tetrachloride administered (CCI4) intraperitoneally. The experiment was performed in two stages. In the first stage, 60 SD rats were divided randomly into normal control group 1(GN1, n=8), hepatic fibrosis group (GC, n=28) and IL-10 intervened group (GI, n=24). At the beginning of the 7th and 11th wk, hepatic stellate cells (HSCs) were isolated, reverse transcription-polymerase chain reation (RT-PCR) and immunocytochemistry were performed to detect the expression of TGF-β1 in HSCs. Histological examination was used to determine the degree of hepatic fibrosis. In the second stage, 47 SD rats were divided randomly into normal control group 2(GN2, n=6) and CCI4 group (GZ, n=41). At the end of the 9th week, rats in GZ group were allocated randomly into model group (GM, n=9), IL-10 treatment group (GT, n=9) and recovered group (GR, n=9). At the end of the 12th week, all rats were sacrificed. RT-PCR and immuno-histochemistry were performed to detect the expression of TGF-β1 in liver tissue. ELISA was used to assay serum TGF-β1 levels. RESULTS: Hepatic fibrosis developed in rats with the increase of the injection frequency of CCI4. In the first stage, hepatic fibrosis developed and HSCs were isolated successfully. At the 7th and 11th week, TGF-β1 mRNA in GC group increased significantly compared with that in GN1(P = 0.001/0.042) and GI groups (P = 0.001/0.007), whereas there was no significant difference between the two groups. The levels of TGF-β1 at the beginning of the 7th wk was higher than that of the 11th wk(P = 0.049). Immunocytochemistry results of TGF-β1 were consistent with the above findings. In the second stage, TGF-β1 increased significantly in GM group compared to GN2. After treatment with IL-10, TGF-β1 declined obviously. The expression of TGF-β1 decreased in GR group but was still higher than that in GT group. CONCLUSION: The levels of TGF-β1 are increased in hepatic fibrosis rats and decreased after treatment with exogenous IL-10. IL-10 may play an anti-fibrotic role by suppressing TGF-β1 expression.
基金
Supported by Natural Science Foundation of Fujian Province, No. 2005D094 and No. C0410025
