热休克蛋白70对感染性脑水肿核转录因子-κB及其抑制蛋白的影响  

Effect of heat shock protein 70 on nuclear factor-κB/inhibitor protein-α of nuclear factor-κB in brain edema induced by infection in rat

作　　者：毛定安[1] 杨于嘉[2] 俞燕[2] 

机构地区：[1]中南大学湘雅二医院儿科,长沙410011 [2]中南大学湘雅医院

出　　处：《中国危重病急救医学》2005年第11期644-646,共3页Chinese Critical Care Medicine

基　　金：国家自然科学基金资助项目(39870251)

摘　　要：目的探讨热休克蛋白70(HSP70)对感染性脑水肿大鼠核转录因子κB(NFκB)活化及NFκB抑制蛋白α(IκBα)的影响及意义。方法制备百日咳菌液大鼠感染性脑水肿模型。72只SD大鼠随机分为对照组(NS组)、感染性脑水肿组(BE组)及热休克处理组(HSP组),各组分别于注射百日咳菌液或生理盐水4、8和24h处死,取脑组织,采用Western印迹杂交分析法检测脑组织HSP70及IκBα表达,凝胶电泳迁移率检测法(EMSA)检测神经细胞核提取物NFκB活性。结果在热休克处理后,HSP组各时间点HSP70表达明显增加,与NS组和BE组比较差异均有显著性(P均<0.01)。在BE组各时间点中,NFκB均显示明显的滞留条带,提示NFκB活性明显增强,而IκBα表达则明显减低。HSP组各时间点中,NFκB滞留条带与BE组比较明显减低,而IκBα表达则明显增强。结论HSP70表达增加可抑制NFκB活化及IκBα蛋白降解,提示HSP70对感染性脑水肿具有保护作用,其机制可能与抑制NFκB活化及IκBα蛋白降解有关。Objective To study the effect of heat shock protein 70 （HSP70） on activation of nuclear factor -κB （NF -κB） and degradation of inhibitor κB-α protein （I -κBα） in brain edema induced by Pertussis bacilli infection in rats. Methods Brain edema was induced by injection of Pertussis bacilli suspension via the left internal carotid artery. Seventy- two Sprague -Dawley rats were divided randomly into brain edema group, pretreatment with heat shock group, and normal saline control group. The rats were sacrificed 4, 8 and 24 hours after injection of Pertussis bacilli and normal saline, respectively. HSPT0 expression and the degradation of I -κBα were assayed in all animals with Western blot analysis. Electrophoretic mobility shift assay （EMSA） was performed to assess NF -κB activation of nuclear extract of neurones. Results The results showed that HSP70 expression was significantly increased in heat shock group compared with control group and brain edema group. The activity of NF - κB started to increase at 2 hours in brain edema group and peaked at 24 hours. The expression of I - κBα began to decrease at 2 hours and reached the lowest level at 24 hours. In heat shock group the activity of NF - κB complexes was lower than that in brain edema group, and the expression of I -κBα higher than that in brain edema group at corresponding time points. Conclusion HSP70 shows a protective effect on development mechanism might be associated with its inhibitory effect of brain edema as its expression increases. The on degradation of I - κBα and activation of NF - κB.

关 键 词：脑水肿 感染性 热休克蛋白 核转录因子-ΚB 核转录因子-κB抑制蛋白-α 

分 类 号：R741[医药卫生—神经病学与精神病学]