Expression of insulin-like growth factor 1 and insulin-like growth factor 1 receptor and its intervention by interleukin-10 in experimental hepatic fibrosis

AIM: To study the expression of IGF-1 and IGF-1R and its intervention by interleuldn-10 in the course of experimental hepatic fibrosis.METHODS: Hepatic fibrosis was induced in rats by carbon tetrachloride intoxication and liver specimens were taken from the rats administered CCl4 with or without IL-10 treatment and the animals of the control group.Immunoreactivities for insulin-like growth factor-1 (IGF-1)and IGF-1 receptor(IGF-1R) were demonstrated by immunohistochemistry, and their intensities were evaluated in different animal groups.RESULTS: The positive levels for IGF-1 and IGF-1R were increased with the development of hepatic fibrosis, with the positive signals localized in cytoplasm and/or at the plasmic membrane of hepatocytes. The positive signals of IGF-1 and IGF-1R were observed more frequently (P<0.01) in the CCl4-treated group (92.0 % and 90.0 %) compared to those in the control group. The positive signals decreased significantly (P<0.05) in IL-10-treated group. The responses in IGF-1 and IGF-1R expression correlated with the time of IL-10 treatment.CONCLUSION: The expression of IGF-1 and IGF-1R immunoreactivities in liver tissue seems to be up-regulated during development of hepatic fibrosis induced by CC14, and exogenic IL-10 inhibits the responses.

AIM:To study the expression of IGF-1 and IGF-1R and its intervention by interleukin-10 in the course of experimental hepatic fibrosis. METHODS:Hepatic fibrosis was induced in rats by carbon tetrachloride intoxication and liver specimens were taken from the rats administered CC14 with or without IL-10 treatment and the animals of the control group. Immunoreactivities for insulin-like growth factor-1 (IGF-1) and IGF-1 receptor(IGF-1R) were demonstrated by immunohistochemistry,and their intensities were evaluated in different animal groups. RESULTS:The positive levels for IGF-1 and IGF-1R were increased with the development of hepatic fibrosis,with the positive signals localized in cytoplasm and/or at the plasmic membrane of hepatocytes.The positive signals of IGF-1 and IGF-1R were observed more frequently (P<0.01) in the CCl4-treated group (92.0 % and 90.0 %) compared to those in the control group.The positive signals decreased significantly (P<0.05) in IL-10-treated group.The responses in IGF-1 and IGF-1R expression correlated with the time of IL-10 treatment. CONCLUSION:The expression of IGF-1 and IGF-1R imrnunoreactivities in liver tissue seems to be up-regulated during development of hepatic fibrosis induced by CCl_4,and exogenic IL-10 inhibits the responses.