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AIM:To study the expression of IGF-1 and IGF-1R and itsintervention by interleukin-10 in the course of experimentalhepatic fibrosis.METHODS:Hepatic fibrosis was induced in rats by carbontetrachloride intoxication and liver specimens were takenfrom the rats administered CC14 with or without IL-10treatment and the animals of the control group.Immunoreactivities for insulin-like growth factor-1 (IGF-1)and IGF-1 receptor(IGF-1R) were demonstrated byimmunohistochemistry,and their intensities were evaluatedin different animal groups.RESULTS:The positive levels for IGF-1 and IGF-1R wereincreased with the development of hepatic fibrosis,with thepositive signals localized in cytoplasm and/or at the plasmicmembrane of hepatocytes.The positive signals of IGF-1and IGF-1R were observed more frequently (P<0.01) in theCCl4-treated group (92.0 % and 90.0 %) compared to thosein the control group.The positive signals decreasedsignificantly (P<0.05) in IL-10-treated group.The responsesin IGF-1 and IGF-1R expression correlated with the time ofIL-10 treatment.CONCLUSION:The expression of IGF-1 and IGF-1Rimrnunoreactivities in liver tissue seems to be up-regulatedduring development of hepatic fibrosis induced by CCl_4,andexogenic 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 carbontetrachloride 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 were demonstrated by immunohistochemistry, and their intensities were evaluated as different animal groups. The positive levels for IGF-1 and IGF-1R were increased with the development of hepatic fibrosis, with thepositive signals localized in cytoplasm and / or at the plasmicmembrane 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 only statistically (P <0.05) in IL-10-treated group. expression correlated with the time of IL-10 treatment. CONCLUSION: The expression of IGF-1 and IGF-1Rimrnunoreactivities in liver tissue seems to be up-regulatedduring development of hepatic fibrosis induced by CCl_4, andexogenic IL-10 inhibits the responses.