摘要
缺血性中风是发达国家死亡率和永久性残疾的主要原因之一。中风诱导大量谷氨酸释放,这反过来导致N-甲基-D-天冬氨酸(NMDA)受体过度激发,因此,神经元中的钙超载通过凋亡级联导致细胞死亡。犬尿氨酸途径是色氨酸分解代谢的复杂酶促级联,产生各种神经活性代谢物。一种代谢产物犬尿喹啉酸(KYNA)是一种有效的内源性NMDA谷氨酸受体拮抗剂,使其成为降低兴奋性毒性和神经炎症的可能治疗工具。最近,临床研究表明,在缺血性中风的急性期,犬尿氨酸途径被激活并且外周水平的代谢物与更差的结果相关。在这篇综述中,我们总结了目前关于犬尿氨酸途径与缺血性卒中关系的文献,并为未来的研究和潜在的药物开发设定了一个方向。
关键词: 犬尿氨酸,中风,缺血,免疫调节,犬尿氨酸类似物,兴奋毒性。
Current Medicinal Chemistry
Title:Ischemic Stroke and Kynurenines: Medicinal Chemistry Aspects
Volume: 25 Issue: 42
关键词: 犬尿氨酸,中风,缺血,免疫调节,犬尿氨酸类似物,兴奋毒性。
摘要: Ischemic stroke is one of the leading causes of mortality and permanent disability in developed countries. Stroke induces massive glutamate release, which in turn causes N-Methyl-D-aspartate (NMDA) receptor over-excitation and thus, calcium overload in neurons leading to cell death via apoptotic cascades. The kynurenine pathway is a complex enzymatic cascade of tryptophan catabolism, generating various neuroactive metabolites. One metabolite, kynurenic acid (KYNA), is a potent endogenous NMDA glutamate receptor antagonist, making it a possible therapeutic tool to decrease excitotoxicity and neuroinflammation. Recently, clinical investigations have shown that during the acute phase of ischemic stroke, kynurenine pathway is activated and peripheral levels of metabolites correlated with worse outcome. In this review, we set out to summarize the current literature on the connection of the kynurenine pathway and ischemic stroke and set a course for future investigations and potential drug development.
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Cite this article as:
Ischemic Stroke and Kynurenines: Medicinal Chemistry Aspects, Current Medicinal Chemistry 2018; 25 (42) . https://dx.doi.org/10.2174/0929867325666180313113411
DOI https://dx.doi.org/10.2174/0929867325666180313113411 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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