Ibuprofen protects ischemia-induced neuronal injury via up-regulating interleukin-1 receptor antagonist expression

被引:46
作者
Park, EM [1 ]
Cho, BP [1 ]
Volpe, BT [1 ]
Cruz, MO [1 ]
Joh, TH [1 ]
Cho, S [1 ]
机构
[1] Cornell Univ, Weill Med Coll, WM Burke Med Res Inst, Dept Neurol & Neurosci, White Plains, NY 10605 USA
关键词
global ischemia; CA1; hippocampus; oxygen glucose deprivation; BV2; microglia; neuroprotection; rat;
D O I
10.1016/j.neuroscience.2005.01.021
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The inflammatory response accompanies and exacerbates the developing injury after cerebral ischemia. Ibuprofen, a non-steroidal anti-inflammatory drug, has been shown to attenuate injuries in animal models of various neurological diseases. In the present study, we investigated ibuprofen's neuroprotective effects in rats exposed to transient forebrain ischemia and in cultures exposed to oxygen glucose deprivation (OGD). Rats treated with ibuprofen after transient forebrain ischemia displayed long-lasting protection of CA1 hippocampal neurons. There were selective increases in interleukin-1 receptor antagonist gene and protein expression in ibuprofen-treated OGD microglia. Furthermore, treatment with ibuprofen in neuron/microglia co-cultures increased the number of surviving HC2S2 neurons against OGD whereas IL-1ra neutralizing antibody reversed the ibuprofen-induced neuroprotection. The data indicate that ibuprofen-induced IL-1ra secretion is involved in neuroprotection against ischemic conditions. (c) 2005 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:625 / 631
页数:7
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