Dynamic expression of MMP-2,TIMP-2 in formation and reversal of experimental hepatic fibrosis in rats

Objective:To establish the model of liver fibrosis(ALF) in rats induced by complex factors,and to discuss the dynamic expression and significance of MMP-2,TIMP-2 in formation and reversal of experimental hepatic fibrosis in rats.Methods: Healthy male rats were divided randomly into two groups: control group(n=10) and liver fibrosis group(n=70).Liver fibrosis model of rat were induced by swine serum,CC14 alcohol and high fat food.Some rats of liver fibrosis group were selected respectively at the 6th,7th,8th to observe their recovery or reversal for 1 month.The expression level of MMP-2,TIMP-2 and histopathological changes of liver tissue were observed at the 1～8th week and of these rats recoverying for 1 month repectively.Results: From the beginning of the 2 th week,the expression level of MMP-2 in liver tissue of the model group went up,and had significant differences compared with that in control group respectively at 2～8th week.Compare with control group,there had no obvious significant differences for TIMP-2 of model group during experiment;The expression level of MMP-2 all went down after recoverying from 3 different time points for 1 month but still higher than normal level.The histopathological changes of liver tissue shows:the hepatocyte of the rats in the liver fibrosis group were vacuolar degeneration widely,Fibroblast hyperplasia were founded between portaltracts.Collagen fibers were founded between hepatic lobules.That is typical change of ALF.At the 8th week,pseudolobuli were founded,cirrhosis was formed.After 1 month recovery from the beginning of the 6th,7th,8th week repectively,there had different degree relieve for ALF.Conclusion: It is successful way to induce ALF in rats by complex factors including alcohol,swine serum,high fat diet and CC14 for 6 week,moreover,the level of expression of MMP-2 was closely related to hepatic fibrosis progress and it may play important role in the formation and reversal of experimental hepatic fibrosis in rats.