Park E-M, Cho B-P, Volpe B T, Cruz M O, Joh T H, Cho S
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, W. M. Burke Medical Research Institute, White Plains, NY 10605, USA.
Neuroscience. 2005;132(3):625-31. doi: 10.1016/j.neuroscience.2005.01.021.
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.
炎症反应伴随着脑缺血后不断发展的损伤并使其恶化。布洛芬作为一种非甾体抗炎药，已被证明可减轻各种神经疾病动物模型中的损伤。在本研究中，我们调查了布洛芬对短暂性前脑缺血大鼠以及氧糖剥夺（OGD）培养物的神经保护作用。短暂性前脑缺血后用布洛芬治疗的大鼠，其海马CA1神经元得到了持久的保护。在布洛芬处理的OGD小胶质细胞中，白细胞介素-1受体拮抗剂基因和蛋白表达有选择性增加。此外，在神经元/小胶质细胞共培养物中用布洛芬处理可增加抵抗OGD存活的HC2S2神经元数量，而白细胞介素-1受体拮抗剂中和抗体则逆转了布洛芬诱导的神经保护作用。数据表明，布洛芬诱导的白细胞介素-1受体拮抗剂分泌参与了针对缺血状况的神经保护作用。
