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首页> 外文期刊>International immunopharmacology >Blockage of P2X7 attenuates acute lung injury in mice by inhibiting NLRP3 inflammasome
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Blockage of P2X7 attenuates acute lung injury in mice by inhibiting NLRP3 inflammasome

机译：P2X7的阻断通过抑制NLRP3炎性体减轻小鼠的急性肺损伤

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摘要

NLRP3 inflammasome is engaged in the inflammatory response during acute lung injury (ALI). Purinergic receptor P2X7 has been reported to be upstream of NLRP3 activation, However, the therapeutic implication of P2X7 in ALI remains to be explored. The present study used lipopolysaccharide (LPS)-induced mouse model to investigate the therapeutic potential of P2X7 blockage in ALL Our results showed that P2X7/NLRP3 inflammasome pathway was significantly upregulated in the lungs of ALI mice as compared with control mice. P2X7 antagonist A438079 suppressed NLRP3/ASC/caspase 1 activation, production of IL-1 beta, IL-17A and IFN-gamma, and neutrophil infiltration but not the production of IL-10, resulting in a significant amelioration of lung injury. Moreover, blockage of P2X7 significantly inhibited NLRP3 inflammasome activation and IL-1 beta production in bone marrow derived macrophages. Similar results were obtained using another P2X7 inhibitor brilliant blue G (BBG) in vivo. Thus, pharmacological blockage of P2X7/NLRP3 pathway can be considered as a potential therapeutic strategy in patients with ALI. (C) 2015 Elsevier B.V. All rights reserved.
机译：NLRP3炎性小体参与急性肺损伤（ALI）期间的炎症反应。嘌呤能受体P2X7已被报道在NLRP3激活的上游，但是，P2X7在ALI中的治疗意义仍有待探索。本研究使用脂多糖（LPS）诱导的小鼠模型研究P2X7阻断对ALL的治疗潜力。我们的结果表明，与对照小鼠相比，ALI小鼠的肺中P2X7 / NLRP3炎性体途径显着上调。 P2X7拮抗剂A438079抑制NLRP3 / ASC / caspase 1活化，IL-1β，IL-17A和IFN-γ的产生以及中性粒细胞浸润，但不抑制IL-10的产生，从而显着改善肺损伤。此外，在骨髓衍生的巨噬细胞中，P2X7的阻断显着抑制了NLRP3炎性小体的活化和IL-1β的产生。使用另一种P2X7抑制剂亮蓝G（BBG）在体内获得了相似的结果。因此，P2X7 / NLRP3途径的药理学阻断可被视为ALI患者的潜在治疗策略。 （C）2015 Elsevier B.V.保留所有权利。

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