Zhonghua nei ke za zhi · 1999
[Intercellular adhesion molecule-1 expression in experimental liver fibrosis].
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Lu L, Zeng M, Fan J, Li J, Liu Y, Ren W, Dai N
Аннотация
OBJECTIVE: To explore the role of intercellular adhesion molecule-1 (ICAM-1) in experimental liver fibrosis.
METHODS: Experimental liver fibrosis models of rats were induced by high fat diet, low fat diet plus ethanol, high fat diet plus ethanol, and carbon tetrachloride subcutaneous injection respectively. At sacrifice, liver pathologic changes were studied and ICAM-1 expression was evaluated with immunohistochemistry by using a monoclonal antibody.
RESULTS: ICAM-1 expression was observed in the hepatocellular membrane; ICAM-1 positive hepatocytes were localized in zones of portal tract with focal necrosis and inflammatory damage. Staining for ICAM-1 was associated with the degree of liver inflammation and fibrosis. In the different models, the intensity of ICAM-1 expression was different; It ranged in an increasing order from high fat diet, low fat diet plus ethanol, high fat diet plus ethanol, and carbon tetrachloride model. The strongest reactivity for ICAM-1 was seen in carbon tetrachloride model (P < 0.05), the difference was significant as compared with the other models. However, there was no significant difference among the three other models (P > 0.05).
CONCLUSION: Upregulation of ICAM-1 expression in experimental liver fibrosis may be related with liver fibrogenesis.
METHODS: Experimental liver fibrosis models of rats were induced by high fat diet, low fat diet plus ethanol, high fat diet plus ethanol, and carbon tetrachloride subcutaneous injection respectively. At sacrifice, liver pathologic changes were studied and ICAM-1 expression was evaluated with immunohistochemistry by using a monoclonal antibody.
RESULTS: ICAM-1 expression was observed in the hepatocellular membrane; ICAM-1 positive hepatocytes were localized in zones of portal tract with focal necrosis and inflammatory damage. Staining for ICAM-1 was associated with the degree of liver inflammation and fibrosis. In the different models, the intensity of ICAM-1 expression was different; It ranged in an increasing order from high fat diet, low fat diet plus ethanol, high fat diet plus ethanol, and carbon tetrachloride model. The strongest reactivity for ICAM-1 was seen in carbon tetrachloride model (P < 0.05), the difference was significant as compared with the other models. However, there was no significant difference among the three other models (P > 0.05).
CONCLUSION: Upregulation of ICAM-1 expression in experimental liver fibrosis may be related with liver fibrogenesis.