The Impact Of PPARγ On INOS And Anti-fibrotic Effect In LX-2Cells

Objective:To study PPARγ and iNOS dynamic changes and relationship in LX-2cells,which explored PPARγ anti-fibrosis mechanism.Methods:Cultured human hepatic stellate cell line.The experiment is divided into fourgroups:1.the control group;2.stimulated by Rosiglitazone group;3.blocked byGW9662group;4.joint experimental group.Four groups were cultured for48hourswith adding the drug intervention.The way of MTT to detect cell proliferationinhibition,using RT-PCR to detect the PPARγ、 iNOS mRNA expression;Nitratereductase method to detect the content of NO;ELISA method to investigate thecontent of type I collagen and α-SMA.Results:1.MTT results:the stimulated by Rosiglitazone group in LX-2cells proliferationsignificantly(0.610±0.063),and compared with the other three groups was significantdifference(P<0.01).2.RT-PCR results:compared with the other three groups was significantly higher(P<0.01);agonist group compared with the other three groups that the expression ofiNOS mRNA significantly reduced (P<0.01); the expression of iNOS and PPARγ mRNAhave a significant negative correlation (correlation index,r=-0.8870,P=0.0080,P<0.01).3.nitrate reductase results:NO content of agonist group(44.89±13.01)μmol/L,significantly lower than the other three groups, there were significant differences(P<0.01).4.ELISA results:the expression of type I collagen and α-SMA in agonist group compared with the other three groups, there were significant differences(P<0.01).Conclusions:PPARγ agonists may increase the expression of PPARγ and inhibit iNOSmRNA to reduce LX-2cells produce NO.Rosiglitazone reduces the expression of type Icollagen and α-SMA, and play anti-fibrosis;Meanwhile,the studies have found iNOSmRNAexpression of PPARγ and has a significant negative correlation.