The Experimental Study Of Reversion In Rat Hepatic Fibrosis And The Intervention Function Of Estradiol

Objective: Some reports have proved that hepaticfibrosis can be reversed. This indicated liver possess thecapacity of removing the fibrosis scar. Hepatic fibrosis modelof spontaneous reversion and no spontaneous reversion wereinduced by the administration of carbon tetrachloride (CCU)in rats. To study the expression of matrix metalloproteinase-2( MMP-2 ) tissue inhibitior of metalloproteinase-1(TIMP-1) and smooth muscle a -actin ( a -SMA) in thelivers of rats with hepatic fibrosis during reversion. Discussthe biology mechanism of mediating reversion.Methods: The study selected male Wistar rats 64,who were divided into two groups randomly.Hepatic fibrosis model of no spontaneous reversion(24):vivo introperitoneally 40%CCl4two times once a week last 20 weeks , 0.1ml/100g once, then 24 rats were divided into four groups randomly, each groups indued 6.The first groups were put to death after vivo introperitoneally 40% CCU 20 weeks ,the second the third and the fourth groups were put to death on 10 20 N 60day after vivo introperitoneally 40%CCl4 20 weeks respectivly. (2) Hepatic fibrosis model of spontaneousreversion(40):vivo introperitoneally 40%CCUtwo times once a week last 4 weeks, the former two weeks 0.2ml/100g once, the later two weeks 0.1ml/100g once. According the time point of spontaneous reversion, 40 rats were divided into four groups randomly, each groups indued 10.The first groups were put to death after vivo introperitoneally 40%CCl4 weeks ^ the second , the third and the fourth groups were put to death on 3 7 28 day after vivo introperitoneally 40%CCl4 four weeks respectivly. Segment of liver left lobe was stabilized by formalinand, which were stroed in hypothermia condition. MMP-2 TIMP-1 a -SMA immunohistochemistry of liver tissue samples were performed and MPIAS-500 multimedia histopathological diagnoses and quantitative analysis for positive cells surface density.Results: Hepatic fibrosis model of no spontaneous reversion, on 60d ,The fibriosis degree have no change and the level of MMP-2 TIMP-1 a -SMA immuno -histochemistry of liver tissue have no change . (2) Hepatic fibrosis model of spontaneous reversion. Histolgical analysis confirmed that the mature collagen fibrosis bridging vascular structures present at 4 week, fibrosis become remodeled during the recovery period, at 4 weeks, There was obvious nodular fibrosis with deposition of well delineated fibrous septae, which were continuous and extended throughout each section, mild fatty change was observed and there was vasculation of hepatocyte . By day 7,the liver appeared to bemore normal histologically, the fibrous septae were less well defined and discontinuous and fewer nodules of regenerative parenchyma were noted. By day 28 ,the fibrous septae had largely resolved and only occational short fibril fragments could be visualized. The level of TIMP-1 a -SMA MMP-2 immunohistochemistry of liver tissue decreased gradually.Conclusions:Hepatic fibrosis model of reversion. With the hepatic fibrosis reversion ,the level of MMP-2 TIMP-1 a -SMA decreased gradually also. (2) Hepatic fibrosis model of no spontaneous reversion, on 60d ,the fibrosis degree have no change and the level of MMP-2 TIMP-1 a -SMA immunohistochemistry of liver tissue have no change .Confirmed the modulation function of TIMP-1 and a -SMA to hepatic fibrosis. Indicated that inhibite TIMP-1 and a -SMA will be key point to treat hepatic fibrosis.