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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
引用本文:毛定安,虞佩兰,杨于嘉.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[J].中国危重病急救医学,2003,15(10):593-595.
作者姓名:毛定安  虞佩兰  杨于嘉
作者单位: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
基金项目: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。

关 键 词:脑水肿  热休克蛋白  白介素-1β  肿瘤坏死因子-α  大鼠
文章编号:1003-0603(2003)10-0593-03
修稿时间:2002年11月7日

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
MAO Ding-an,YU Pei-lan,YANG Yujia..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[J].Chinese Critical Care Medicine,2003,15(10):593-595.
Authors:MAO Ding-an  YU Pei-lan  YANG Yujia
Institution:Department of Neurology, Jiangxi Children Hospital, Nanchang 330006, Jiangxi, China.
Abstract:OBJECTIVE: To investigate the changes of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) 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-1beta and TNF-alpha 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-alpha 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-1beta were significantly increased in IBE group compared with NS group at 4 hours, 8 hours. HSR reduced the IL-1beta and TNF-alpha concentrations in the brain tissue in compared with IBE group (P<0.05 or P<0.01). CONCLUSION: IL-1beta and TNF-alpha are involved in infectious brain edema by IBE. HSP70 against infectious brain edema in rats may be associated with the reduction of IL-1beta and TNF-alpha in brain tissue.
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