摘要
目的观察高迁移率族蛋白B1(HMGB1)、核转录因子(NF-κB)在心肺复苏术后大鼠海马组织内的表达,以期探讨其可能意义。方法 40只SD大鼠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48h各时间点分为5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,RT-PCR和Western Blot检测HMGB1、NF-κB水平表达,并对二者进行相关分析。结果病理切片显示假手术组海马结构未见明显变化,复苏组存在缺血病理改变,24h最为显著,48h损伤仍比较重;与假手术组比较,复苏组海马HMGB1、NF-κB mRNA表达均呈先上升后下降的趋势,均于24h达峰值(P<0.01);复苏组HMGB1蛋白表达在自主循环恢复后2h显著降低,24h达到峰值,在48h稍下降,差异均有统计学意义(P<0.01);HMGB1和NF-κB蛋白表达呈显著正相关。结论 HMGB1/NF-κB信号通路可能参与心肺复苏术后早期脑炎性损伤,干预此通路的靶向性治疗有望减轻心肺复苏术后脑炎性损伤。
Objective To observe the changes of high mobility group box 1（HMGB1）and nuclear factorκB（NF-κB）expression in the hippocampus of rats after cardiopulmonary resuscitation so as to unravel the role of HMGB1 and NF-κB in neuroin flammation.Methods Totally 40Sprague-Dawley rats were randomly divided into shame-operated group and recover group[including2,6,12,24 and 48hof 5sub-groups after restoration of spontaneous circulation（ROSC）].The animals were sacrificed and hippocampus 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 hand still obviously at ROSC 48 htime 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 24h（P〈0.01）,much higher than that of shame-operated group;the HMGB1 level in the hippocampus of rats after recover significantly declined at 2hafter ROSC and increased obviously at 6,12 hand reached peak 24 hlater,then decreased 48hlater（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.
出处
《重庆医学》
CAS
北大核心
2015年第32期4483-4486,共4页
Chongqing medicine
基金
江苏省连云港市科技局科研基金资助项目(sh1001)
