摘要
目的:建立简单、易复制的幼年鼠内毒素性脑水肿模型,并从Ca^(2+)、钙调素(CaM)水平探讨脑水肿的发生发展。方法:45只幼鼠,随机分内毒素组(36只)和对照组(9只),分别于腹腔内注射内毒素(LPS)10mg/kg和等容量生理盐水,并用电镜观察其病理、用常规生化法测定脑含水量和伊文氏蓝(EB)含量、用荧光标记术和免疫印迹法分别测定脑组织细胞内[Ca^(2+)]和CaM表达。结果:脑组织含水量和EB含量显著高于对照组;细胞内[Ca^(2+)]明显增高,脑组织CaM表达增强;电镜显示血脑屏障(Blood-brain barrier,BBB)受损、神经元变性、胶质细胞肿胀、坏死等特征。结论:LPS导致了BBB通透性改变,并引起了混合性脑水肿。LPS引起了细胞内[Ca^(2+)]增高,并激活了CaM,从而启动了Ca^(2+)-CaM信号通路,这可能与其增加BBB通透性并导致脑水肿形成有密切关系。
Objective :To establish a simple, reproducible brain edema model induced by endotoxin in infant rats and explore the role of intracellular free calcium and calmodulin (CaM). in the development of brain edema. Methods: A total of 45 infant rats were divided randomly into endotoxin treated( n = 36) and control( n = 9) group. The animals were intraperitoneally injected with 10mg/kg of endotoxin or saline respectively. The brain tissue intracelluar free [Ca2 + ] as well as the expression of CaM was detected by fluorescence and protein hybridizaton methods respectively. The tissue water content,Evans Blue content and pathology under electronic microscope were also observed. Results:Brain water and EB content were remarkably increased in endotoxin treated animals compared with those in the control, in which the intracellular free [Ca2+ ] was also significantly increased and the expression of CaM up - regulated. Electron microscopic studies revealed that the blood - brain barrier(BBB)was disrupted with neuronal degeneration,neurogliocyte swelling and necrosis. Conculsion :These results suggest that LPS increases the intracellular free [Ca2+ ] ,and activates the CaM - dependent function via Ca2+ /CaM pathway,which might relate to the increased BBB permeability and brain edema formation.
出处
《重庆医科大学学报》
CAS
CSCD
2003年第1期53-56,共4页
Journal of Chongqing Medical University
