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[热应激诱导热休克蛋白70抑制感染性脑水肿大鼠脑组织中白细胞介素-1β和肿瘤坏死因子-α水平]

[Heat shock protein 70 induction by heat stress suppress interleukin-1beta and tumor necrosis factor-alpha levels in the brain tissue in rats with infectious brain edema].

作者信息

Mao Ding-an, Yu Pei-lan, Yang Yu-jia

机构信息

Department of Neurology, Jiangxi Children Hospital, Nanchang 330006, Jiangxi, China.

出版信息

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2003 Oct;15(10):593-5.

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.

摘要

目的

通过热应激反应(HSR)研究感染性脑水肿(IBE)大鼠脑组织中白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的变化及其与热休克蛋白70(HSP70)的关系。

方法

将72只SD大鼠随机分为正常对照组(NS组)、IBE组和HSP组,每组再分为三个亚组。分别于注射IBE或生理盐水后4小时、8小时和24小时处死各亚组大鼠。采用蛋白质免疫印迹分析法测定脑组织中HSP70的含量。采用酶联免疫吸附测定法(ELISA)测定大鼠脑匀浆中IL-1β和TNF-α的浓度。

结果

结果显示,热休克后脑组织中HSP70含量升高。IBE组和NS组在4小时、8小时、24小时时HSP70均诱导至基础水平。IBE组各时间点TNF-α浓度均显著高于NS组(P<0.01或P<0.05),尤其是在第8小时。IBE组在4小时、8小时时IL-1β浓度与NS组相比显著升高。与IBE组相比,热应激反应降低了脑组织中IL-1β和TNF-α的浓度(P<0.05或P<0.01)。

结论

IL-1β和TNF-α参与了IBE所致的感染性脑水肿。HSP70对大鼠感染性脑水肿的保护作用可能与降低脑组织中IL-1β和TNF-α的浓度有关。

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