Expression of Insulin-like Growth Factor 1 and Its Intervention by Inter-leukin-10 in Experimental Hepatic Fibrosis
Lijuan Zhang
Abstract
Lijuan Zhang
Abstract
Objective: To study the expression of IGF-1 and its intervention by IL-10 in the course of experimental hepatic fibrosis. Methods: Experimental rat hepatic fibrosis model induced by CCl4 was established and the liver tissues were obtained from the control group, the model group and the IL-10 treated group in different period respectively. The expression of IGF-1 in different group and different phase in the development of hepatic fibrosis was measured by S-P immunohistochemistry. Results: The CCl4-induced experimental rat hepatic fibrosis model was established successfully. The positive expression of IGF-1 was increased obviously with the development of hepatic fibrosis, and the positive expression was mainly in the plasma and/or the membrane of hepatocytes. Ridit analysis indicated that there was significant difference between the positive expression of IGF-1 in control group (38.1%) and that in model group (92.0%, P0.01), the positive expression in IL-10 treated group (71.4%) was decreased when compared with control group (P0.05), and the positive expression decreasing gradually with the increasing IL-10 treatment time. Conclusion: The positive expression of IGF-1 in liver tissue was increased with the development of hepatic fibrosis, and ectogenic IL-10 restrained the expression of IGF-1 in liver fibrosis induced by CCl4.
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Objective: To study the expression of IGF-1 and its intervention by IL-10 in the course of experimental hepatic fibrosis. Methods: Experimental rat hepatic fibrosis model induced by CCl4 was established and the liver tissues were obtained from the control group, the model group and the IL-10 treated group in different period respectively. The expression of IGF-1 in different group and different phase in the development of hepatic fibrosis was measured by S-P immunohistochemistry. Results: The CCl4-induced experimental rat hepatic fibrosis model was established successfully. The positive expression of IGF-1 was increased obviously with the development of hepatic fibrosis, and the positive expression was mainly in the plasma and/or the membrane of hepatocytes. Ridit analysis indicated that there was significant difference between the positive expression of IGF-1 in control group (38.1%) and that in model group (92.0%, P0.01), the positive expression in IL-10 treated group (71.4%) was decreased when compared with control group (P0.05), and the positive expression decreasing gradually with the increasing IL-10 treatment time. Conclusion: The positive expression of IGF-1 in liver tissue was increased with the development of hepatic fibrosis, and ectogenic IL-10 restrained the expression of IGF-1 in liver fibrosis induced by CCl4.
Key concepts: Hepatic fibrosis, CCL4, Fibrosis, Immunohistochemistry, Internal medicine, Insulin-like growth factor, Medicine, Growth factor