Interleukin-1β potentiates neuronal injury in a variety of injury models involving energy deprivation

被引：26

作者：

Fogal, B ^{[1
]}

Hewett, JA ^{[1
]}

Hewett, SJ ^{[1
]}

机构：

[1] Univ Connecticut, Ctr Hlth, Dept Neurosci, Farmington, CT 06030 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2005年 / 161卷 / 1-2期

关键词：

interleukin-1; beta; hypoxia; glucose deprivation; oxygen-glucose deprivation; neuronal injury; cortex;

D O I：

10.1016/j.jneuroim.2004.12.007

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

The purpose of this study was to develop a suitable in vitro model system to study the biochemical pathway(s) by which interleukin-1 beta (IL-1 beta) contributes to the pathogenesis of cerebral ischemia. Thus, the effect of IL-1 beta on a number of injury paradigms associated with energy deprivation was investigated using murine mixed cortical cell cultures. While IL-1 beta by itself was not neurotoxic, pre-treatment but not concurrent or post-treatment-with this cytokine potentiated neuronal injury induced by depriving cultures of either oxygen, glucose, or both oxygen and glucose. Cytotoxicity was abolished by an IL-1 beta-neutralizing antibody. Together, these results demonstrate the establishment of reliable and reproducible in vitro models that will now allow detailed investigation of the cellular and molecular mechanisms relating to IL-1 beta-mediated neuronal cell death. (C) 2005 Elsevier B.V. All rights reserved.

引用

页码：93 / 100

页数：8

共 51 条

[1]

Interleukin-1β and interleukin-1 receptor antagonist do not affect glutamate release or calcium entry in rat striatal synaptosomes [J].