TITLE

Nuclear factor KB inactivation in the rat liver ameliorates short term total warm ischaemia/reperfusion injury

AUTHOR(S)
Suetsugu, H.; Limuro, Y.; Ueharo, T.; Nishio, T.; Harada, N.; Yoshida, M.; Hatano, E.; Son, G.; Fujimoto, J.; Yamaoka, Y.
PUB. DATE
June 2005
SOURCE
Gut;Jun2005, Vol. 54 Issue 6, p835
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: In hepatic ischaemia/reperfusion injury, activated liver macrophages (Kupffer cells) are dominantly regulated by a transcription factor, nuclear factor κB (NFκB), with respect to expression of inflammatory cytokines, acute phase response proteins, and cell adhesion molecules. Aims: We assessed whether inactivation of NF; in the liver could attenuate total hepatic warm ischaemia/reperfusion injury. Methods: We studied rats with hepatic overexpression of inhibitor κBα super-repressor (lκBα SR) caused by a transgene introduced using an adenoviral vector. Hepatic ischaemia/reperfusion injury was induced under warm conditions by total occlusion of hepatoduodenal ligament structures for 20 minutes, followed by reperfusion. Controls included uninfected and control virus (AdLacZ) infected rats. Results: lκBα SR was overexpressed in Kupffer cells as well as in hepatocytes, blocking nuclear translocation of NFκB (p65) into the nucleus after reperfusion. Gene transfection with IκBα SR, but not with LacZ, markedly attenuated ischaemia/reperfusion injury, suppressing inducible nitric oxide synthase and nitrotyrosine expression in the liver. Moreover, no remarkable hepatocyte apoptosis was detected under IκBα SR overexpression. Conclusions: Adenoviral transfer of the lκBα SR gene in the liver ameliorates short term warm ischaemia/ reperfusion injury, possibly through attenuation of hepatic macrophage activation.
ACCESSION #
17176786

 

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