Interleukin‐1β but not tumor necrosis factor‐α potentiates neuronal damage by quinolinic acid: Protection by an adenosine A2A receptor antagonist
Interleukin‐1β but not tumor necrosis factor‐α potentiates neuronal damage by quinolinic acid: Protection by an adenosine A2A receptor antagonist
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白细胞介素-1β（而非肿瘤坏死因子-α）增强了喹啉酸对神经元的损伤：腺苷 A2A 受体拮抗剂的保护作用
DOI：
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
W. Behan
中科院分区：
文献类型：
--
作者：
T. Stone;W. Behan
喹啉酸是对N-甲基-D-天冬氨酸（NMDA）敏感的谷氨酸受体的激动剂。它与感染、创伤和缺血相关的神经功能障碍有关，尽管其神经毒性相对较低。本研究旨在检查喹啉酸与促炎细胞因子白细胞介素-1 β（IL-1β）和肿瘤坏死因子-α（TNF-α）的联合作用。将化合物施用于麻醉的雄性大鼠的海马体，使动物恢复7天，然后对海马体进行组织学分析，通过计数完整的健康神经元来估计神经元损伤。低剂量的喹啉酸或IL-1β本身不会造成损伤，但两者共同诱导海马锥体神经元的显著损失。较高剂量几乎完全丧失锥体细胞。海马内TNF-α单独没有产生作用，但显著减少了喹啉酸产生的神经元损失。腺苷A2 A受体拮抗剂ZM 241385减少了喹啉酸和IL-1β组合产生的神经元损失。结果表明，同时喹啉酸和IL-1β，都是由脑感染或损伤诱导的，在神经元损伤的产生中是协同作用的，并且可以一起显著地导致创伤性、感染性或缺血性脑损伤。腺苷A2 A受体的拮抗作用保护神经元免受喹啉酸和IL-1β的组合。© 2007 Wiley利斯公司
Quinolinic acid is an agonist at glutamate receptors sensitive to N‐methyl‐D‐aspartate (NMDA). It has been implicated in neural dysfunction associated with infections, trauma, and ischemia, although its neurotoxic potency is relatively low. This study was designed to examine the effects of a combination of quinolinic acid and the proinflammatory cytokines interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α). Compounds were administered to the hippocampus of anesthetized male rats, animals being allowed to recover for 7 days before histological analysis of the hippocampus for neuronal damage estimated by counting of intact, healthy neurons. A low dose of quinolinic acid or IL‐1β produced no damage by itself, but the two together induced a significant loss of pyramidal neurons in the hippocampus. Higher doses produced almost total loss of pyramidal cells. Intrahippocampal TNF‐α produced no effect alone but significantly reduced the neuronal loss produced by quinolinic acid. The adenosine A2A receptor antagonist ZM241385 reduced neuronal loss produced by the combinations of quinolinic acid and IL‐1β. The results suggest that simultaneous quinolinic acid and IL‐1β, both being induced by cerebral infection or injury, are synergistic in the production of neuronal damage and could together contribute substantially to traumatic, infective, or ischemic cerebral damage. Antagonism of adenosine A2A receptors protects neurons against the combination of quinolinic acid and IL‐1β. © 2007 Wiley‐Liss, Inc.
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内源性 55 kDa TNF 受体介导神经细胞系中的细胞死亡。
DOI：
10.1016/0169-328x(95)00310-o
发表时间：
1996
期刊：
Brain research. Molecular brain research
影响因子：
--
作者：
Sipe,KJ;Srisawasdi,D;Dantzer,R;Kelley,KW;Weyhenmeyer,JA
通讯作者：
Weyhenmeyer,JA
影响因子：
5
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D. V. von Lubitz;R. Lin;K. Jacobson
通讯作者：
D. V. von Lubitz;R. Lin;K. Jacobson
影响因子：
4.4
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I. Chung;E. Benveniste
DOI：
10.1073/pnas.86.16.6348
发表时间：
1989-08-01
影响因子：
11.1
作者：
LIEBERMAN, AP;PITHA, PM;SHIN, ML
通讯作者：
SHIN, ML
受损脊髓中喹啉酸的积累：大鼠和豚鼠之间的时间过程、分布和物种差异。
DOI：
10.1089/neu.1997.14.89
发表时间：
1997
期刊：
Journal of neurotrauma.
影响因子：
--
作者：
Blight,AR;LeroyJr,EC;Heyes,MP
通讯作者：
Heyes,MP