Purinergic receptor modulation of BV-2 microglial cell activity: Potential involvement of p38 MAP kinase and CREB
Purinergic receptor modulation of BV-2 microglial cell activity: Potential involvement of p38 MAP kinase and CREB
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DOI：
10.1016/j.jneuroim.2005.05.012
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发表时间：
2005-09-01
影响因子：
3.3
通讯作者：
Watters, JJ
中科院分区：
文献类型：
--
作者：
Brautigam, VM;Frasier, C;Watters, JJ
脑损伤后的细胞外液中存在丰富的ATP，它对小胶质细胞具有强大的调节作用，小胶质细胞的过度激活被认为会加剧神经元损伤。我们在这里表明，ATP通过一种涉及p38 MAP激酶的机制，降低了lps刺激的BV-2小胶质细胞中iNOS和COX-2的表达，并减少了NO的释放。此外，我们证明ATP对NO产生的抑制作用发生在暴露30分钟内，并与转录因子CREB的激活相关。综上所述，这些数据表明ATP可能通过一种涉及p38/CREB通路增强激活的机制在大脑中发挥神经保护作用。(C) 2005 Elsevier B.V.版权所有
ATP is abundant in the extracellular fluid following brain injury, and it exerts potent modulatory effects on microglia, whose hyperactivation is thought to exacerbate neuronal damage. We show here that ATP decreases LPS-stimulated iNOS and COX-2 expression and reduces NO release in BV-2 microglia by a mechanism involving p38 MAP kinase. Further, we demonstrate that the inhibitory effects of ATP on NO production occur within 30 min of exposure and correlate with activation of the transcription factor CREB. Together, these data suggest that ATP may exert neuroprotective effects in the brain via a mechanism involving augmented activation of the p38/CREB pathway. (C) 2005 Elsevier B.V. All rights reserved.