新数据表明氧化型三磷酸腺苷（ATP）具有更广泛的作用机制：P2X7受体并非唯一靶点。
Novel data point to a broader mechanism of action of oxidized ATP: the P2X7 receptor is not the only target.
作者信息
Di Virgilio Francesco
机构信息
Department of Experimental and Diagnostic Medicine, University of Ferrara, Via Borsari 46, I-44100 Ferrara, Italy.
出版信息
Br J Pharmacol. 2003 Oct;140(3):441-3. doi: 10.1038/sj.bjp.0705469.
Abstract
Oxidized ATP (oATP) is a Schiff-base-forming reagent that has been used for some years as an antagonist at the P2X7 receptor (P2X7R). Preincubation of mononuclear phagocytes with this inhibitor leads to attenuation of several proinflammatory responses triggered by extracellular ATP as well as a few non-nucleotide agonists. Novel data show that oATP reduces NFkappaB activation and IL-8 release in cells lacking P2X7R, thus suggesting that some anti-inflammatory effects of oATP may not be due to blockade of the P2X7R. This effect of oATP resembles the action of other natural or synthetic Schiff-base-forming reagents with immunomodulatory activity.
摘要
氧化型三磷酸腺苷（oATP）是一种能形成席夫碱的试剂，多年来一直被用作P2X7受体（P2X7R）的拮抗剂。用这种抑制剂对单核吞噬细胞进行预孵育会导致细胞外ATP以及一些非核苷酸激动剂引发的多种促炎反应减弱。新数据表明，oATP可降低缺乏P2X7R的细胞中NFκB的激活和白细胞介素-8的释放，因此提示oATP的某些抗炎作用可能并非归因于对P2X7R的阻断。oATP的这种作用类似于其他具有免疫调节活性的天然或合成席夫碱形成试剂的作用。
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本文引用的文献
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Oxidized ATP (oATP) attenuates proinflammatory signaling via P2 receptor-independent mechanisms.氧化型三磷酸腺苷（oATP）通过不依赖P2受体的机制减弱促炎信号传导。
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