摘要
目的研究谷氨酸对脑缺血性损害引起的肠炎性反应的影响。方法成年雄性SD大鼠接受15 min双侧颈总动脉夹闭,造成局灶性脑缺血损伤,缺血同时腹腔内注射大剂量谷氨酸单钠。在缺血-再灌注后6 h分别收集血浆和小肠组织,用酶联免疫吸附法(ELISA)测定血浆和肠组织中的肿瘤坏死因子α(TNF-α)含量;用[32磷]-ATP标记核因子-κB(NFκ-B)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。实验当中,连续监测血液动力学参数改变并记录。结果脑的短暂性缺血可引起肠TNFα-含量的轻度增加,而谷氨酸单钠可引起肠中的TNF-α含量显著增加;缺血联合应用谷氨酸单钠可使肠中的TNF-α含量较单独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。在整个实验过程中,各组平均动脉压和心率基本保持在基线水平。结论大量谷氨酸可增加肠的炎症反应;谷氨酸增加肠的炎性反应主要通过激活NF-κB信号转导途径而实现的。
Objective To study the modulation of glutamate on post-ischemic intestinal inflammatory responses, Methods Adult male SD rats were subjected to 15 min of bilateral carotid artery clamping and injection of monosodium glutamate （MSG） intraperitoneally, and decapitating at selected time points. Tumor necrosis factor alpha （TNF-α） production and nuclear factor kappa B （NF-kB） activity were determined by enzyme-linked immunosorbanee assay （ELISA） and eleetrophoretie mobility shift assay （EMSA） respectively. Hemodynamic parameters were monitored continuously during cerebral ischemia and reperfusion. Results The rats subjected transient cerebral ischemia showed a minor increase of TNF-α production in intestinal tissue. MSG-treated rats displayed a significant high level of TNF-α in intestinal tissue. Rats treated with both cerebral ischemia and MSG showed significant low level of TNF-α in intestinal tissue compared with those of MSG-treated rats, These results correlated significantly with NF-kB production calculated within the same time window. During exper iment, mean blood pressure and heart rate were stable in all groups. Conclusions The results suggest the involvement of glutamate in the mechanism of intestinal inflammation responses. The effect of glutamate on intestinal inflammatory responses after ischemia is up-regulation at the transcriptional level, predominatly through NF-kB signal transduction pathway.
出处
《临床麻醉学杂志》
CAS
CSCD
2006年第2期121-124,共4页
Journal of Clinical Anesthesiology
基金
国家自然科学基金资助项目(No.30070731)
关键词
脑缺血-再灌注
谷氨酸
肠
炎症介质
Brain ischemia-reperfusion
Glutamate
Intestine
Inflammation mediators
