title: Effect of heat shock preconditioning on NF-kappaB/I-kappaB pathway during I/R injury of the rat liver.
abstract: Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication after liver surgery. Heat shock (HS) preconditioning is an effective strategy for protecting the liver from I/R injury, but its exact mechanism is still unclear. Because the activation of nuclear factor-kappaB (NF-kappaB) is an important event in the hepatic I/R-induced inflammatory response, the effect of HS preconditioning on the pathway for NF-kappaB activation was investigated. In the control group, NF-kappaB was activated 60 min after reperfusion, but this activation was suppressed in the HS group. Messenger RNA expressions of proinflammatory mediators during reperfusion were also reduced with HS preconditioning. Concomitant with NF-kappaB activation, NF-kappaB inhibitor I-kappaB proteins were degraded in the control group, but this degradation was suppressed in the HS group. This study shows that HS preconditioning protected the liver from I/R injury by suppressing the activation of NF-kappaB and the subsequent expression of proinflammatory mediators through the stabilization of I-kappaB proteins.
authors.affiliation: Department of Gastroenterological Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606 - 8507, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Uchinami
authors.forename: Yuzo
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Makoto
authors.initials: M
authors.lastname: Kume
authors.forename: Kei
authors.initials: K
authors.lastname: Yonezawa
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Kojiro
authors.initials: K
authors.lastname: Taura
authors.forename: Akio
authors.initials: A
authors.lastname: Nakajima
authors.forename: Koichiro
authors.initials: K
authors.lastname: Hata
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000818:Animals; D054426:Chemokine CXCL2; D018925:Chemokines / Q000235:genetics; D015870:Gene Expression / Q000276:immunology; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D018869:Heat-Shock Response / Q000276:immunology; D020672:I-kappa B Proteins / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D019194:Ischemic Preconditioning; D008099:Liver / Q000276:immunology / Q000378:metabolism*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat