Objective To observe the changes of high mobility group box 1(HMGB1) and nuclear factorκB(NF‐κB) expres‐sion in the hippocampus of rats after cardiopulmonary resuscitation so as to unravel the role of HMGB 1 and NF‐κB in neuroin flam‐mation .Methods Totally 40 Sprague‐Dawley rats were randomly divided into shame‐operated group and recover group [including 2 ,6 ,12 ,24 and 48 h of 5sub‐groups after restoration of spontaneous circulation (ROSC)] .The animals were sacrificed and hippo‐campus were removed at the indicated time .Pathological changes were observed at each time point .The expression of HMGB1 and NF‐κB were determined using RT‐PCR and Western blot respectively .Results There were no histopathological in the hippocampus of rats in shame‐operated group ,brain tissue appeared change of ischemia pathology in recover group ,it was the most severest at ROSC 24 h and still obviously at ROSC 48 h time point .HMGB1 mRNA and NF‐κB mRNA expression in the hippocampus of rats of recover group increased obviously along with the prolongation of time following ROSC and reached its peak at ROSC 24 h(P<0 . 01) ,much higher than that of shame‐operated group ;the HMGB1 level in the hippocampus of rats after recover significantly de‐clined at 2 h after ROSC and increased obviously at 6 ,12 h and reached peak 24 h later ,then decreased 48 h later(P<0 .01) ,there was positive correlation between the expression of HMGB1 and NF‐κB protein .Conclusion HMGB1/NF‐κB signaling pathway may play an important role in the early stages of brain injury after cardiopulmonary resuscitation .Targeted therapies of this path way would be possible to open a new avenue for preventing neuroinflammation after recover .

Objective_To investigate the role of HMGB1 involved in the activation of P38MAPK signal pathway in the hippocampus of rats after cardiopulmonary resuscitation.Methods_Rats were randomly divided into two groups as shame-operated group, CPR group including 2, 6, 12, 24 and 48 h after restoration of spontaneous circulation ( ROSC) (5sub-groups) .The animals were sacrificed and hippocampus were removed at the indicated time.Patholog-ical changes were examined at each time point.Calculated the brain water content by day/wet ration.The HMGB1 mRNA expression was detected by RT-PCR technique.The expressions of HMGB1 and P38MAPK activity were deter-mined using Western blot.Results_There were no histopathological change in the hippocampus of rats in shame-op-erated group, brain tissue appeared change of ischemia pathology in CPR group, it was the most severest at ROSC 24 h.The brain water content, HMGB1 mRNA in rats of CPR group increased obviously along with the prolongation of time following ROSC and reached its peak at ROSC 24 h(P<0.01),much higher than that of shame-operated group, the HMGB1 level in the hippocampus of rats after CPR significantly declined at 2 h after ROSC(P<0.01)and increased obviously at 6, 12 h and reached peak 24 h later(P<0.01), the P38MAPK activity in the hippo-campus of rats after CPR, significantly increased at 2 h after ROSC and reached peak 6 h later(P<0.01), then declined slowly later, much higher than that of shame-operated group.Conclusions_HMGB1 involved in the acti-vation of P38 MAPK signal pathway may play an important role in the early stages of brain injury after CPR.