CAJ | 학술논문

目的：探讨高迁移率族蛋白B1（HMGB1）在心肺复苏（CPR）术后大鼠海马组织激活P38 MAPK信号通路的作用。方法将SD大鼠随机分为假手术组和复苏组（按复苏后自主循环恢复后2、6、12、24和48 h各时间点分5个亚组）。在相应的时间点断头处死，取海马组织，HE染色观察海马病理变化，干湿称重法测定脑组织含水量，RT－PCR法检测HMGB1 mRNA表达，Western blot检测HMGB1和P38激酶活性。结果假手术组海马组织结构未见明显变化，复苏组存在缺血病理改变，24 h最为显著。与假手术组比较：复苏组脑组织含水量、海马HMGB1 mRNA表达均呈先上升后下降的趋势，于24 h达到峰值（ P＜0．01）；复苏组HMGB1表达在ROSC后2 h显著降低，6和12 h逐渐增高，24 h达到峰值（P＜0．01）；复苏组海马组织P38激酶活性于2 h表达显著升高（P＜0．01），6 h达到高峰（P＜0．01），后缓慢下降。结论 HMGB1可能通过参与P38 MAPK信号通路的激活介导CPR术后早期脑组织炎性反应损伤。
목적：탐토고천이솔족단백B1（HMGB1）재심폐복소（CPR）술후대서해마조직격활P38 MAPK신호통로적작용。방법장SD대서수궤분위가수술조화복소조（안복소후자주순배회복후2、6、12、24화48 h각시간점분5개아조）。재상응적시간점단두처사，취해마조직，HE염색관찰해마병리변화，간습칭중법측정뇌조직함수량，RT－PCR법검측HMGB1 mRNA표체，Western blot검측HMGB1화P38격매활성。결과가수술조해마조직결구미견명현변화，복소조존재결혈병리개변，24 h최위현저。여가수술조비교：복소조뇌조직함수량、해마HMGB1 mRNA표체균정선상승후하강적추세，우24 h체도봉치（ P＜0．01）；복소조HMGB1표체재ROSC후2 h현저강저，6화12 h축점증고，24 h체도봉치（P＜0．01）；복소조해마조직P38격매활성우2 h표체현저승고（P＜0．01），6 h체도고봉（P＜0．01），후완만하강。결론 HMGB1가능통과삼여P38 MAPK신호통로적격활개도CPR술후조기뇌조직염성반응손상。
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.