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首页> 外文期刊>Life sciences >Prostaglandin E-2 deteriorates N-methyl-D-aspartate receptor-mediated cytotoxicity possibly by activating EP2 receptors in cultured cortical neurons
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Prostaglandin E-2 deteriorates N-methyl-D-aspartate receptor-mediated cytotoxicity possibly by activating EP2 receptors in cultured cortical neurons

机译：前列腺素E-2可能通过激活培养的皮层神经元中的EP2受体来恶化N-甲基-D-天冬氨酸受体介导的细胞毒性

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摘要

The activation of glutamate receptors, particularly N-methyl-D-aspartate (NMDA) receptors, initiates ischemic cascade in the early stages of cerebral ischemia. Postischemia, cerebral ischemia is also associated with an inflammatory reaction that contributes to tissue damage. The upregulation of neuronal cyclooxygenase-2 (COX-2) and elevation of prostaglandin E-2 (PGE(2)) have been reported to occur after cerebral ischemic insult. We therefore studied whether the COX-2 reaction product PGE(2) affects glutamate receptor-mediated cell death in cultured rat cortical cells. PGE2 was found to augment NMDA-mediated cell death. The transcription of EP1, EP2, EP3 and EP4 PGE2 receptor genes was investigated using reverse transcriptase-polymerase chain reaction (RT-PCR). EP1, EP2 and EP3 receptor genes were found in cortical cells. Butaprost (an EP2 agonist) markedly enhanced NMDA-mediated cell death, whereas 17-phenyl trinor-PGE(2) (an EP1 agonist) and sulprostone (an EP3 agonist) had little effect. Both PGE(2) and butaprost elevated cAMP intracellular levels in the cortical cells; moreover, forskolin, an activator of adenylate cyclase, enhanced NMDA-mediated cell death. These results suggest that PGE(2), acting via EP2 receptors, aggravates excitotoxic neurodegeneration by a cAMP-dependent mechanism. (c) 2005 Elsevier Inc. All rights reserved.
机译：谷氨酸受体，特别是N-甲基-D-天冬氨酸（NMDA）受体的活化，在脑缺血的早期阶段引发缺血级联反应。缺血后，脑缺血也与导致组织损伤的炎症反应有关。据报道，在脑缺血后，神经元环氧合酶2（COX-2）上调和前列腺素E-2（PGE（2））升高。因此，我们研究了COX-2反应产物PGE（2）是否影响培养的大鼠皮质细胞中谷氨酸受体介导的细胞死亡。发现PGE2增加了NMDA介导的细胞死亡。使用逆转录聚合酶链反应（RT-PCR）研究了EP1，EP2，EP3和EP4 PGE2受体基因的转录。在皮层细胞中发现了EP1，EP2和EP3受体基因。 Butaprost（一种EP2激动剂）显着增强了NMDA介导的细胞死亡，而17-苯基trinor-PGE（2）（一种EP1激动剂）和sulprostone（一种EP3激动剂）几乎没有作用。 PGE（2）和butaprost均可升高皮质细胞中的cAMP细胞内水平;此外，福司可林，腺苷酸环化酶的激活剂，增加了NMDA介导的细胞死亡。这些结果表明，PGE（2）通过EP2受体起作用，通过cAMP依赖性机制加重了兴奋毒性神经变性。 （c）2005 Elsevier Inc.保留所有权利。

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