| Objective To explore the effects of 17 β -estradiol (E2) in rat liver fibrosis.Methods 40 male rats were divided into 4 groups, including group A, B, C and D. Liver fibrosis was induced in all male rats by CCL4 administration. Rats in group A were treated with E2(2mg/kg) twice a week from the third week to the eighth week; Rats in group B were treated with E2(1mg/kg) twice a week from the third week to the eighth week; Rats in group C were control group; Rats in group D were treated with tamoxifen (6mgAg) every day orally from the third week to the eighth week. All the rats were killed at the 8th week. Then we collected the portal vein blood and liver tissue for our research working. We detected the rat serum estradiol level by radioimmunoassay, the rat hepatocyte pathological change by using light microscope to observe the liver HE stained paraffin section, the expressions of HGF mRNA, NF-kappa Bp65mRNA, Endostatin mRNA and VEGF165mRNA in rat livers by real-time PCR (SYBER GREEN 1), the expressions of HGF, PCNA, NF-kappa Bp65, ICAM-1, Endostatin and VEGF165 in all rat liver by immunohistochemistry, and the titer of AECA in rat livers by indirect immunofluorescence test.Results (1)The serum E2 levels of all groups were detected as: A>B >D>C, and total comparisons of above four groups were statistically significant (P<0.05); But the levels of E2 between C and D groups were not statistically significant(P>0.05). (2)The cellular ratio of hepatocyte steatosis and necrosis in all rat were increasing progressively as: A |
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