摘要
目的探讨热应激反应对大鼠感染性脑水肿的保护机制。方法将大鼠进行热休克预处理后，采用百日咳菌液所致的感染性脑水肿模型，观察脑匀浆上清液中肿瘤坏死因子α（ＴＮＦα）、一氧化氮（ＮＯ）水平的变化。结果感染性脑水肿的脑组织含水量、脑匀浆ＴＮＦα含量及ＮＯ浓度均增高，热休克预处理可降低脑组织含水量、ＴＮＦα含量及ＮＯ浓度；脑组织含水量与ＴＮＦα含量及ＮＯ浓度呈正相关，相关系数分别为０．４５８和０．７６２。结论热应激反应能减轻感染性脑水肿的发生，其机理可能与ＨＳＰ７０表达增加。
Objective The study was to explore the protective mechanism of heat stress response against infectious brain edema in rats.Methods An animal model of infectious brain edema by pertussis bacilli was used after heat stress response.The concentrations of tumor necrosis factorα(TNF-α) and nitric oxide (NO) in the brain homogenate of rats were determined.Results that TNFα level and NO level in infectious brain edema significantly elevated.The two parameters were markedly fell in heat stress pretreatment group,and all these variations were significantly correlated with those of brain water content.Conclusion The results suggest the protective mechanism of heat stress response against infectious brain edema in rats may be associated with enhancement heat shock protein 70 gene expression and the reduction of TNF-α and NO levels.
出处
《中风与神经疾病杂志》
CSCD
北大核心
1998年第4期198-200,共3页
Journal of Apoplexy and Nervous Diseases
关键词
脑水肿
热激反应
肿瘤坏死因子Α
一氧化氮
Brain edema Heat stress response Tumor necrosis factorα Nitric oxide Rat
