2003World Journal of GastroenterologyOpen access

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

Xiaozhong Wang

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Abstract

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 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 CCl(4), and exogenic IL-10 inhibits the responses.

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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 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 CCl(4), and exogenic IL-10 inhibits the responses.

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Available abstract

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 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 CCl(4), and exogenic IL-10 inhibits the responses.

Key concepts: Internal medicine, Hepatic fibrosis, Endocrinology, Insulin-like growth factor, Fibrosis, Immunohistochemistry, Growth factor, Receptor

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