Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion 英文参考文献.docVIP

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Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion 英文参考文献.doc

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Oxidation of HMGB1 Causes Attenuation of Its Pro-Inflammatory Activity and Occurs during Liver Ischemia and Reperfusion 英文参考文献

OxidationofHMGB1CausesAttenuationofItsPro- InflammatoryActivityandOccursduringLiverIschemia andReperfusion AndingLiu1,2,3.,HaoshuFang1,3.,OlafDirsch4,HaoJin1,3,UtaDahmen1,3 * 1Experimental Transplantation Surgery, Department of General, Visceral and Vascular Surgery, Friedrich-Schiller-University Jena, Jena, Germany, 2The Centre for Molecular Medicine, Shaoxing People’s Hospital, the First Affiliated Hospital of Shaoxing University, Shaoxing, PR China, 3Department of General, Visceral and TransplantationSurgery,UniversityHospitalEssen,UniversityofDuisburgandEssen,Essen,Germany,4InstituteforPathology,UniversityHospitalofJena,Jena,Germany Abstract Highmobilitygroupbox1(HMGB1)isanucleartranscriptionfactor.OnceHMGB1isreleasedbydamagedcellsoractivated immune cells, it acts as danger molecule and triggers the inflammatory signaling cascade. Currently, evidence is accumulating that posttranslational modifications such as oxidation may modulate the pro-inflammatory potential of dangersignals.WehypothesizedthatoxidationofHMGB1mayreduceitspro-inflammatorypotentialandcouldtakeplace during prolonged ischemia and upon reperfusion. Liver grafts were cold preserved for 24h and flushed with saline in hourlyintervalstocollecttheeffluent.Livergrafts,cold-preservedfor6h,weretransplantedintosyngeneicrecipientsto obtainserumandliversamples24hafterinitiationofreperfusion.Additionoftheeffluenttoamacrophagecultureinduced the synthesis of tumor necrosis factor-alpha (TNF-a) and interleukin (IL)-6. The stimulatory activity of graft effluent was reducedafter depletion ofHMGB1via immunoprecipitation. Oxidation oftheeffluent HMGB1 usingH2O2 attenuatedits stimulatory activity as well. Liver transplantation of cold preserved grafts caused HMGB1 translocation and release as determined by immunohistochemistry and ELISA-assay, respectively. Using Western blot with non-reducing conditions revealedthepresenceofoxidizedHMGB1inliversamplesobtainedafter12handineffluentsamplesafter16hofcold preservatio