The Effect Of I Kappa B And Nuclear Factor Kappa B In Immune Liver Injury

Objective The transcription factor, nuclear factor kappa B(NF-KB) and its inhibitory protein I kappa B were found to be involved in many pathophysiology processes such as immunity, inflammation and cancer. To further elucidate the relevance of NF-KB and IKB for liver damage , we investigated the roles of them in the immune liver injury model induced by ConA. Methods 1) The first group: male BALB/c mouse were mock-treated with PBS. 2)The second group: mouse were challenged by a single tail intravenous injection of ConA(20mg/kg) at the time points indicated. The third group: mouse were treated with PDTC(120mg/kg) 30 minuts before ConA injection. 2) NF-KB , IKB and induced nitric oxide synthase (iNOS) were determined by western blotting. TNF a in serum and tissue were measured and the level of nirric oxide(NO) in liver tissue was determined. 3) The levels of necrosis and apoptosis were determined by histological examination and DNA ladder. Results Treatment of mice with 20mg/kg ConA resulted in apoptosis and necrosis. ConA administration also caused increases in hepatic TNF a expression, as well as inducible nitric oxide synthase expression. This was correlated with increases in serum ALT levels, degradation of IB and the activation of NF-KB in liver tissue. PDTC can inhibit the IB degradation and the translocation of NF-KB to the nuclear.Correspondingly , the levels of TNF a and NO reduced,and thenecrosis and apoptosis were prevented.Conclusion The results demonstrate that IB and NF-KB regulate some gene expression such as TNF α , iNOS in vivo, thereby contributing to immune liver injury.