摘要
Objective:To observe the expression level of TNF-α mRNA in rats with hepatic fibrosis induced by dimethylnitrosamine (DMN) and to explore its relationship with collagen metabolism and its diagnostic value for hepatic fibrosis.Methods: Twenty-five male Wistar rats were randomly divided into normal control group (n=10) and model group (n=15). Model rats were induced by DMN for 4 weeks and at final stage were executed. TNF-α mRNA were detected by RT-PCR and the inflammatory necrosis and collagen deposition in hepatic tissue were observed by HE stain and Sirius red stain. The liver functions were determined by automatic biochemical analytic device. The serum marks of liver fibrosis, such as HA, LN and Ⅳ-C were measured with ELISA and RIA. Results: In this study, the rat model of liver fibrosis induced by DMN was successfully constructed. RT-PCR reveals that TNF-α mRNA expression in control group is lower than that of model group. The liver functions of model group were impaired compared with those of the control group (P<0.01). Semi-quantitive analysis revealed that TNF-α/β-actin of normal rats was 0.39±0.12, while 0.93±0.05 of model rats. The concentration of HA (434.44±98.81 vs 252.9±26.59 ng/ml, P<0.01), LN (70.67±6.32 vs 37.90±5.97 ng/ml, P<0.01) and Ⅳ-C (79.39±10.52 vs 21.40±4.17 ng/ml, P<0.01) were significantly increased in the model group as well. Changes of the indexes were similar to the pathological damage of the liver. Conclusion: The results suggested that activation of TNF-α in liver tissues may be the common pathogenic mechanism of liver fibrosis. TNF-α may be a useful index for the diagnosis of hepatic fibrosis which worthies further investigation.
Objective：To observe the expression level of TNF-α mRNA in rats with hepatic fibrosis induced by dimethylnitrosamine （DMN） and to explore its relationship with collagen metabolism and its diagnostic value for hepatic fibrosis.Methods： Twenty-five male Wistar rats were randomly divided into normal control group （n=10） and model group （n=15）. Model rats were induced by DMN for 4 weeks and at final stage were executed. TNF-α mRNA were detected by RT-PCR and the inflammatory necrosis and collagen deposition in hepatic tissue were observed by HE stain and Sirius red stain. The liver functions were determined by automatic biochemical analytic device. The serum marks of liver fibrosis, such as HA, LN and Ⅳ-C were measured with ELISA and RIA. Results： In this study, the rat model of liver fibrosis induced by DMN was successfully constructed. RT-PCR reveals that TNF-α mRNA expression in control group is lower than that of model group. The liver functions of model group were impaired compared with those of the control group （P〈0.01）. Semi-quantitive analysis revealed that TNF-α/β-actin of normal rats was 0.39±0.12, while 0.93±0.05 of model rats. The concentration of HA （434.44±98.81 vs 252.9±26.59 ng/ml, P〈0.01）, LN （70.67±6.32 vs 37.90±5.97 ng/ml, P〈0.01） and Ⅳ-C （79.39±10.52 vs 21.40±4.17 ng/ml, P〈0.01） were significantly increased in the model group as well. Changes of the indexes were similar to the pathological damage of the liver. Conclusion： The results suggested that activation of TNF-α in liver tissues may be the common pathogenic mechanism of liver fibrosis. TNF-α may be a useful index for the diagnosis of hepatic fibrosis which worthies further investigation.
