Increasing evidence has revealed that neuroinflammation plays a pivotal role in axonal injures. Nucleotide oligomerization domain (NOD)-like receptor protein (NLRP3) inflammasome is reported to be widely involved with the pathology of central nervous system disorders. But the role of NLRP3 in diffuse axonal injury (DAI) are rarely reported. The purpose of this study was to investigate the expression of NLRP3 after diffuse axonal injury and the role of NLRP3 in axonal injures. The lateral head rotation device was used to establish DAI model of rats. Immunohistochemical staining for β-amyloid precursor protein and Bielschowsky silver staining were used to assess axonal injures and axonal loss. Terminal Deoxynucleotidyl Transferase-Mediated Digoxigenin-dUTP-Biotin Nick-End Labelling Assay was used to detect cell apoptosis. Brain water content was used to assess cerebral edema and the modified Neurologic Severity Score was used to assess the neurological deficits. Components of NLRP3 inflammasome, such as NLRP3, apoptosis-associated speck-like (ASC) adapter protein and caspase-1, and pro-inflammatory cytokines, for example IL-18 and IL-1β, were over-expressed in early stages of DAI. MCC950, a selective small-molecule inhibitor of NLRP3 inflammasome, inhibited the over-expression of NLRP3 inflammasome and pro-inflammatory cytokines after DAI. MCC950 alleviated axonal injures and cell apoptosis. MCC950 also decreased brain water content and alleviated neurologic deficits 1 day and 3 days after DAI but not 7 days after DAI. These results suggest that MCC950 treatment in the early stages of DAI has a time limiting effect in preventing from axonal injuries and neurological deficits, and that NLRP3 inflammasome plays an important role in axonal injures and may be a potential candidate for axonal injures following DAI.

越来越多的证据表明，神经炎症在轴突损伤中起关键作用。据报道，核苷酸寡聚结构域 (NOD) 样受体蛋白 (NLRP3) 炎性体广泛参与中枢神经系统疾病的病理学。但很少报道 NLRP3 在弥漫性轴索损伤 (DAI) 中的作用。本研究旨在探讨弥漫性轴索损伤后NLRP3的表达及NLRP3在轴索损伤中的作用。采用侧头旋转装置建立大鼠DAI模型。β-淀粉样前体蛋白的免疫组织化学染色和 Bielschowsky 银染色用于评估轴突损伤和轴突损失。末端脱氧核苷酸转移酶介导的地高辛-dUTP-生物素尼克末端标记测定用于检测细胞凋亡。脑含水量用于评估脑水肿，修改后的神经严重程度评分用于评估神经功能缺损。NLRP3 炎性体的成分，例如 NLRP3、凋亡相关斑点样 (ASC) 衔接蛋白和 caspase-1，以及促炎细胞因子，例如 IL-18 和 IL-1β，在 DAI 的早期过度表达. MCC950 是 NLRP3 炎性体的选择性小分子抑制剂，可抑制 DAI 后 NLRP3 炎性体和促炎细胞因子的过度表达。MCC950 减轻轴突损伤和细胞凋亡。MCC950 在 DAI 后 1 天和 3 天（但不是在 DAI 后 7 天）也降低了脑含水量并减轻了神经功能缺损。