BACKGROUND Inflammasomes are large intracellular multi-protein signaling complexes that are formed in the cytosolic compartment as an inflammatory immune response to endogenous danger signals. The formation of the inflammasome enables activation of an inflammatory protease caspase-1 and pyroptosis initiation with the subsequent cleaving of the pro-inflammatory cytokines interleukin (IL)-1β and proIL-18 to produce active forms. The inflammasome complex consists of a nod-like receptor, the adapter apoptosis-associated speck-like protein, and caspase-1. Dysregulation of NLRP3 inflammasome activation is involved in neuroinflammation disease pathogenesis, although its role in SCI development and progression remains controversial due to the inconsistent findings described. SUMMARY In this review, we summarize the current knowledge on the contribution of the NLRP3 inflammasome on potential neuroinflammation diseases therapy.

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NLRP3 炎症小体在神经炎症疾病中的作用

背景炎症小体是大的细胞内多蛋白信号复合物，其在胞质区室中形成，作为对内源性危险信号的炎症免疫反应。炎性体的形成能够激活炎性蛋白酶 caspase-1 和细胞焦亡，随后促炎性细胞因子白细胞介素 (IL)-1β 和 proIL-18 被裂解以产生活性形式。炎性体复合物由一个 nod 样受体、适配器凋亡相关斑点样蛋白和 caspase-1 组成。NLRP3 炎症小体激活的失调参与神经炎症疾病的发病机制，尽管由于所描述的不一致发现，其在 SCI 发展和进展中的作用仍存在争议。总结 在本次审查中，