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白细胞介素-1参与脑缺血的潜在机制。

Potential mechanisms of interleukin-1 involvement in cerebral ischaemia.

作者信息

Touzani O, Boutin H, Chuquet J, Rothwell N

机构信息

School of Biological Sciences, University of Manchester, UK.

出版信息

J Neuroimmunol. 1999 Dec;100(1-2):203-15. doi: 10.1016/s0165-5728(99)00202-7.

DOI:10.1016/s0165-5728(99)00202-7
PMID:10695731
Abstract

Interleukin-1 (IL-1) has pleiotropic actions in the central nervous system. During the last decade, a growing corpus of evidence has indicated an important role of this cytokine in the development of brain damage following cerebral ischaemia. The expression of IL-1 in the brain is dramatically increased during the early and chronic stage of infarction. The most direct evidence that IL-1 contributes significantly to ischaemic injury is that (1) central administration of IL-1beta exacerbates brain damage, and (2) injection or over-expression of interleukin-1 receptor antagonist, and blockade of interleukin-1beta converting enzyme activity reduce, dramatically, infarction and improve behavioural deficit. The mechanisms underlying IL-1 actions in stroke are not definitively elucidated, and it seems likely that its effects are mediated through stimulation and inhibition of wide range of pathophysiological processes.

摘要

白细胞介素-1(IL-1)在中枢神经系统中具有多效性作用。在过去十年中,越来越多的证据表明这种细胞因子在脑缺血后脑损伤的发展中起重要作用。在梗死的早期和慢性阶段,IL-1在脑中的表达显著增加。IL-1对缺血性损伤有显著作用的最直接证据是:(1)脑室内注射IL-1β会加重脑损伤;(2)注射或过度表达白细胞介素-1受体拮抗剂以及阻断白细胞介素-1β转化酶活性可显著减少梗死面积并改善行为缺陷。IL-1在中风中的作用机制尚未完全阐明,其作用似乎是通过刺激和抑制多种病理生理过程来介导的。

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