热休克蛋白70对感染性脑水肿大鼠白介素和肿瘤坏死因子的影响及意义  

Heat shock protein 70 induction by heat stress suppress interleukin-1β and tumor necrosis factor-α levels in the brain tissue in rats with infectious brain edema

作　　者：毛定安[1] 虞佩兰[2] 杨于嘉[2] 

机构地区：[1]江西省儿童医院神经内科,江西南昌330006 [2]中南大学湘雅医院儿科,湖南长沙410008

出　　处：《中国危重病急救医学》2003年第10期593-595,共3页Chinese Critical Care Medicine

基　　金：国家自然科学基金资助项目 ( 3 9870 2 5 1)

摘　　要：目的 :探讨白介素和肿瘤坏死因子在感染性脑水肿时的变化及热休克蛋白 70 (HSP70 )对它们的影响。方法 :将 72只 SD大鼠随机分为正常对照组 (NS)、感染性脑水肿组 (IBE)和热休克处理组 (HSP) ,每组又分为 4、8和 2 4 h3个时间点亚组。采用 Western印迹杂交技术检测各组各时间点的 HSP70的表达 ,采用酶联免疫吸附法 (EL ISA)分别检测 3组大鼠脑组织匀浆中白介素 1β(IL 1β)及肿瘤坏死因子α(TNFα)的含量。结果 :Western印迹杂交分析经密度扫描后结果表明 ,感染性脑水肿及正常大鼠脑组织内均有一定量的 HSP70表达 ,而 HSP组的 HSP70量明显高于 IBE组 (P均 <0 .0 1)。与 NS组比较 ,4、8和 2 4 h IBE组的 TNFα含量明显增加 ,以 8h为最明显 (P均 <0 .0 1) ;而在 4和 8h IBE组中 ,脑组织 IL 1β含量明显增高 ,以 8h增高最明显 (P均 <0 .0 1) ,2 4 h则明显下降 ;热休克反应能降低 IL 1β及 TNFα在脑组织中的含量 (P<0 .0 5或P<0 .0 1)。结论 :IL 1β及 TNFα参与了感染性脑水肿的病理过程 ,HSP70能减轻感染性脑水肿的机制可能与其抑制 IL 1β和 TNFα生成有关。Objective: To investigate the changes of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) in the brain tissue of rats with infectious brain edema(IBE) and their relationship with heat shock protein 70(HSP70) by heat stress response(HSR). Methods:Seventy-two SD rats were randomly divided into normal controls group(NS group), IBE group, and HSP group, each group was divided into three subgroups. The rats in subgroups were killed at 4 hours, 8 hours and 24 hours after the injections of IBE or normal saline respectively. HSP70 in brain tissues were determined by Western blot analysis. The concentrations of IL-1β and TNF-α in the brain homogenate of rats were determined by enzyme linked immunoadsorbent assay(ELISA). Results: The results showed that HSP70 in brain tissues were elevated after heat shock. IBE group and NS group at 4 hours, 8 hours, 24 hours were induced to base levels of HSP70. The concentrations of TNF-α were significantly elevated in IBE group than in NS group at the various time points (P<0.01 or P<0.05), especially at 8 hours. The concentrations of IL-1β were significantly increased in IBE group compared with NS group at 4 hours, 8 hours. HSR reduced the IL-1β and TNFα concentrations in the brain tissue in compared with IBE group (P<0.05 or P<0.01). Conclusion:IL-1β and TNF-α are involved in infectious brain edema by IBE. HSP70 against infectious brain edema in rats may be associated with the reduction of IL-1β and TNF-α in brain tissue.

关 键 词：脑水肿 热休克蛋白 白介素-1Β 肿瘤坏死因子-α 大鼠 

分 类 号：R741[医药卫生—神经病学与精神病学]