Inhibition of Fas/FasL mRNA expression and TNF-a release in concanavalin A-induced liver injury in m

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:hblhzl_18
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AIM:Bicyclol,4,4’-dimethoxy-5,6,5’,6’-dimethylene-dioxy-2-hydroxymethyl-2’-carbonyl biphenyl,is a new anti-hepatitisdrug.The aim of the present study was to investigate theprotective effect of bicyclol on concanavalin A(Con A)-inducedimmunological liver injury in mice and its mechanism.METHODS:Liver injury was induced by injection of Con Avia tail vein of mice and assessed biochemically andhistologically.Serum transaminase and tumor necrosis factoralpha(TNF-α)were determined.Liver lesions were observedby light microscope.Expressions of TNF-α,interferon gamma(IFN-γ),Fas and Fas ligand(FasL)mRNA in the livers weremeasured by RT-PCR.RESULTS:Serum transaminase level and liver lesions inCon A-induced mice were markedly reduced by oraladministration of 100,200 mg/kg of bicyclol.TNF-α level inserum was also reduced by bicyclol.Con A injection inducedup-regulation of TNF-α,IFN-γ,Fas and FasL mRNA expressionin liver tissues.Bicyclol significantly down-regulated theexpression of IFN-γ,Fas and FasL mRNA,but only slightlyaffected TNF-α mRNA expression in liver tissues.CONCLUSION:Bicyclol protects against Con A-induced liverinjury mainly through inhibition of Fas/FasL mRNA expressionin liver tissues and TNF-α release in mice. AIM: Bicyclol, 4,4’-dimethoxy-5,6,5 ’, 6’-dimethylene-dioxy-2-hydroxymethyl- 2’-carbonyl biphenyl, is a new anti-hepatitis drug. The aim of the present study was to investigate the role of bicyclol on concanavalin A (Con A) -inducedimmunological liver injury in mice and its mechanism. METHODS: Liver injury was induced by injection of Con Avia tail vein of mice and assessed biochemically andhistologically. Serum transaminase and tumor necrosis factoralpha (TNF -α) were determined by light microscope. Expressions of TNF-α, interferon gamma (IFN-γ), Fas and Fas ligand (FasL) mRNA in the livers were by by RT-PCR .RESULTS: Serum transaminase level and Liver lesions in CON A-induced mice were markedly reduced by oladdin of 100, 200 mg / kg of bicyclol.TNF-α level in serum also also reduced by bicyclol.Con A inducibledup-regulation of TNF-α, IFN-γ, Fas and FasL mRNA expressionin liver tissues.Bicyclol significantly down-regulated theexpression of IFN-γ, Fas and FasL mRNA, but only slightly affected TNF-α mRNA expression in liver tissues. CONCLUSION: Bicyclol protects against Con A-induced liver in jury mainly through inhibition of Fas / FasL mRNA expression in liver tissues and TNF-α release in mice.
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