Rosiglitazone For LX-2Cells PPAR Gamma And NF-kappa B MRNA Expression

Objective:To investigate the effects of Rosiglitazone on the LX-2cellproliferation and the expression of mRNA of NF-κB and PPARγ in LX-2in vitro.Methods: After treatment with different concentration of rosiglitazone(0μmol/L,1μmol/L，5μmol/L，10μmol/L，20μmol/L，25μmol/L，50μmol/L，100μmol/L) for48h, the status of LX-2proliferation was measured by the CCK8assay, the level of type I collagen in cell culture supernatant were detected byELISA,RT-PCR detect the expression of NF-κB and PPARγ mRNA.Results:①CCK8assay results showed that rosiglitazone in LX-2cellsproliferation inhibition of case,the drug concentration of1μmol/L，5μmol/L，10μmol/L，20μmol/L，25μmol/L，50μmol/L，100μmol/L,the inhibition rate were8.29%，14.43%，16.23%，18.29%，27.01%，34.67%，39.48%.The rosiglitazonesignificantly inhibits the proliferation of HSC in a dose dependent manner.②Compared with the control group, the expression of mRNA of NF-κB and PPARγ ofLX-2in vitro in the Rosiglitazone treatment group significantly.(NF-κB/β-actionmRNA:1.091±0.045vs0.557±0.035;PPARγ/β-actionmRNA:0.979±0.015vs1.621±0.046).There was significant difference between the two groupsP<0.05.And NF-κ BmRNA and PPARγmRNA expression was significantlyassociated with the existence of the relationship(correlation index was:-0.951,p=0.000，P<0.01)③ELISA results showed that the expression of type I collagen inrosiglitazone group were decreased compared to blank control group(P<0.05).Conclusion:Rosiglitazone which is PPARγ agonist can inhibit the proliferationof LX-2cells, upregulating the expression of PPARγmRNA,downregulating theexpression of NF-κBmRNA and type I collagen. There is correlation between theinfluence of rosiglitazone on the expression of PPARγ and NF-κB.