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Anesth Analg. 2004 Mar;98(3):768-74, table of contents. doi: 10.1213/01.ane.0000099720.25581.86.
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N-methyl-D-aspartate receptor and L-type voltage-gated Ca2+ channel activation mediate proline-rich tyrosine kinase 2 phosphorylation during cerebral ischemia in rats.N-甲基-D-天冬氨酸受体和L型电压门控Ca2+通道激活介导大鼠脑缺血期间富含脯氨酸的酪氨酸激酶2磷酸化。
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Glutamate activates NF-kappaB through calpain in neurons.谷氨酸通过钙蛋白酶在神经元中激活核因子κB。
Eur J Neurosci. 2003 Dec;18(12):3305-10. doi: 10.1111/j.1460-9568.2003.03079.x.
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Effect of excess extracellular glutamate on dendrite growth from cerebral cortical neurons at 3 days in vitro: Involvement of NMDA receptors.体外培养3天时细胞外谷氨酸过量对大脑皮质神经元树突生长的影响：N-甲基-D-天冬氨酸受体的作用
J Neurosci Res. 2003 Dec 1;74(5):688-700. doi: 10.1002/jnr.10797.
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Serum tumor necrosis factor-alpha, glutamate and lactate changes in two different stages of mechanical intestinal obstruction.
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The distinct role of mGlu1 receptors in post-ischemic neuronal death.代谢型谷氨酸受体1（mGlu1）在缺血后神经元死亡中的独特作用。
Trends Pharmacol Sci. 2003 Sep;24(9):461-70. doi: 10.1016/S0165-6147(03)00231-1.
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The two faces of IKK and NF-kappaB inhibition: prevention of systemic inflammation but increased local injury following intestinal ischemia-reperfusion.IKK和核因子κB抑制的两面性：预防全身炎症，但肠道缺血再灌注后局部损伤增加。
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Gabexate mesilate, a synthetic protease inhibitor, inhibits lipopolysaccharide-induced tumor necrosis factor-alpha production by inhibiting activation of both nuclear factor-kappaB and activator protein-1 in human monocytes.甲磺酸加贝酯是一种合成的蛋白酶抑制剂，通过抑制人单核细胞中核因子-κB和活化蛋白-1的激活，抑制脂多糖诱导的肿瘤坏死因子-α的产生。
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谷氨酸对局灶性脑缺血后肠道和大脑炎症反应的影响。

Effect of glutamate on inflammatory responses of intestine and brain after focal cerebral ischemia.

作者信息

Xu Lei, Sun Jie, Lu Ran, Ji Qing, Xu Jian-Guo

机构信息

Department of Anesthesiology, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.

出版信息

World J Gastroenterol. 2005 Feb 7;11(5):733-6. doi: 10.3748/wjg.v11.i5.733.

DOI:10.3748/wjg.v11.i5.733
PMID:15655833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4250750/
Abstract

AIM

To study the modulation of glutamate on post-ischemic intestinal and cerebral inflammatory responses in a ischemic and excitotoxic rat model.

METHODS

Adult male rats were subjected to bilateral carotid artery occlusion for 15 min and injection of monosodium glutamate intraperitoneally, to decapitate them at selected time points. Tumor necrosis factor alpha (TNF-alpha) level and nuclear factor kappa B (NF-kappaB) activity were determined by enzyme-linked immunosorbant assay (ELISA) and electrophoretic mobility shift assay (EMSA), respectively. Hemodynamic parameters were monitored continuously during the whole process of cerebral ischemia and reperfusion.

RESULTS

Monosodium glutamate (MSG) treated rats displayed statistically significant high levels of TNF-alpha in cerebral and intestinal tissues within the first 6 h of ischemia. The rats with cerebral ischemia showed a minor decrease of TNF-alpha production in cerebral and intestinal tissues. The rats with cerebral ischemia and treated with MSG displayed statistically significant low levels of TNF-alpha in cerebral and intestinal tissues. These results correlated significantly with NF-kappaB production calculated at the same intervals. During experiment, the mean blood pressure and heart rates in all groups were stable.

CONCLUSION

Glutamate is involved in the mechanism of intestinal and cerebral inflammation responses. The effects of glutamate on cerebral and intestinal inflammatory responses after ischemia are up-regulated at the transcriptional level, through the NF-kappaB signal transduction pathway.

摘要

目的

在缺血和兴奋性毒性大鼠模型中研究谷氨酸对缺血后肠道和脑炎症反应的调节作用。

方法

成年雄性大鼠接受双侧颈动脉闭塞15分钟并腹腔注射谷氨酸，在选定时间点断头。分别通过酶联免疫吸附测定（ELISA）和电泳迁移率变动分析（EMSA）测定肿瘤坏死因子α（TNF-α）水平和核因子κB（NF-κB）活性。在脑缺血和再灌注的全过程中持续监测血流动力学参数。

结果

谷氨酸钠（MSG）处理的大鼠在缺血的最初6小时内，脑和肠道组织中的TNF-α水平在统计学上显著升高。脑缺血大鼠的脑和肠道组织中TNF-α产生略有下降。脑缺血并接受MSG处理的大鼠脑和肠道组织中的TNF-α水平在统计学上显著降低。这些结果与相同时间间隔计算的NF-κB产生显著相关。实验期间，所有组的平均血压和心率均稳定。

结论

谷氨酸参与肠道和脑炎症反应机制。缺血后谷氨酸对脑和肠道炎症反应的影响通过NF-κB信号转导途径在转录水平上上调。