论文部分内容阅读
:探讨热休克反应 (HSR)对百日咳杆菌所致的大鼠感染性脑水肿诱生型一氧化氮合酶 (iNOS)mRNA表达的影响。方法 :从大鼠左侧颈内动脉注入百日咳菌液制备感染性脑水肿 (感脑 )模型 ,采用组织细胞原位杂交技术检测脑组织iNOSmRNA的表达。结果 :生理盐水组、4h感脑组及 4h热休克处理组均未见iNOSmRNA表达 ,8h ,2 4h时感染性脑水肿组均有明显的杂交信号 ,以 2 4h更为明显 ;而 8h ,2 4h热休克处理组仅有少数细胞有阳性信号。结论 :热休克反应对感染性脑水肿的保护作用可能与抑制iNOSmRNA的表达有关
: To investigate the effect of heat shock response (HSR) on the expression of inducible nitric oxide synthase (iNOS) mRNA of Bordetella pertussis-induced rat cerebral edema. Methods: Infectious cerebral edema (sensory brain) model was induced by intraperitoneal injection of pertussis into rat left internal carotid artery. The expression of iNOS mRNA in brain tissue was detected by in situ hybridization. Results: No iNOS mRNA expression was found in the normal saline group, 4 h sensory brain group and 4 h heat shock treatment group, and obvious hybridization signals were observed in the infected cerebral edema group at 8 and 24 h 4h heat shock treatment group only a few cells have a positive signal. Conclusion: The protective effect of heat shock on infectious brain edema may be related to inhibiting the expression of iNOS mRNA