谷氨酸增加脑缺血-再灌注损伤后脑和肠的炎性反应  

Glutamate up-regulates inflammatory responses of intestine and brain after focal cerebral ischemia

作　　者：徐磊[1] 孙杰[1] 吕然[1] 嵇晴[1] 徐建国[1] 

机构地区：[1]南京军区南京总医院麻醉科,江苏南京210002

出　　处：《医学研究生学报》2007年第9期912-915,919,共5页Journal of Medical Postgraduates

基　　金：国家自然科学基金资助项目(批准号:30070731)

摘　　要：目的:采用脑缺血联合兴奋毒性动物模型研究谷氨酸对脑缺血性损害引起的脑和肠炎性反应的影响。方法:成年雄性SD大鼠接受15min双侧颈总动脉夹闭,造成脑的局灶性缺血损伤,缺血组和对照组腹腔内分别注射大剂量谷氨酸单钠,监测血流动力学参数改变并记录;在缺血后6 h分别收集血浆、大脑和小肠组织,用酶联免疫吸附法(ELISA)测定血浆、脑和肠组织中的肿瘤坏死因子-α(TNF-α)含量;用32P-ATP标记核因子-κB(NF-κB)寡核苷酸探针,聚丙烯酰胺凝胶电泳成像组织中的NF-κB,计算机软件半定量分析NF-κB活性变化,并和非注药组进行对比。结果:脑缺血后脑和肠中的TNF-α含量轻度增加,而谷氨酸单钠可引起脑和肠中的TNF-α含量显著增加;缺血组应用谷氨酸单钠可使脑和肠中的TNF-α含量较对照组应用谷氨酸单钠时显著减低,NF-κB活性检测结果与TNF-α含量变化相一致。结论:谷氨酸可增加脑和肠的炎性反应,这可能是通过激活NF-κB信号转导途径来实现的。Objective： To study the regulatory effect of glutamate on post-ischemia intestinal and cerebral inflammatory responses in a model of ischemic and excitotoxic insults. Methods： Adult male rats were subjected to 15-min tamping of bilateral carotid arteries and intraperitoneal injection of monosodium glutamate（MSG）. Hemodynamic parameters were continuously during the whole course of the induced cerebral ischemia. Six hours later, plasma and cerebral and intestinal tissues were collected, and values of tumor necrosis factor alpha （TNF-α） and the activity of nuclear factor kappa B （NF-κB） were determined by enzyme-linked immunosorbance assay （ELISA） and electrophoretic mobility shift assay （EM- SA） respectively. Results ： The rats treated with MSG displayed statistically higher levels of TNF-α in the cerebral and intestinal tissues than the controls （P 〈 0.05 ）, while those treated with both cerebral ischemia and MSG showed significantly lower levels of TNF-α than the MSG-treated ones （ P 〈 0.05 ）, with a good correlation between TNF-α values and NF-κB activities. Conclusion：Glutamate up-regulates cerebral and intestinal inflammatory responses after ischemia, probably through the NF-κB signal transduction pathway.

关 键 词：兴奋性氨基酸 脑缺血 再灌注 肿瘤坏死因子-α 核因子-ΚB 

分 类 号：R743.31[医药卫生—神经病学与精神病学]