作　　者： ; ;

机构地区： 华南理工大学医学院

出　　处： 《中华神经科杂志》 2020年第2期147-151,共5页

摘　　要： 帕金森病是一种常见的神经退行性疾病,其特征是黑质多巴胺能神经元的进行性丧失。虽然帕金森病的病因可能是多因素的,但神经炎症是该疾病发病机制的重要组成部分。核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体是调节炎症的多蛋白先天免疫复合物。在帕金森病神经炎症中,NLRP3炎性小体复合物组装募集并激活半胱氨酸天冬氨酸蛋白酶-1(caspase-1),激活的caspase-1切割炎性因子白细胞介素-1β和白细胞介素-18的前体,从而启动下游炎性级联反应,加重多巴胺神经元损伤。本综述中对NLRP3炎性小体在帕金森病病理生物学中最新研究进行总结,并且讨论了通过抑制NLRP3炎性小体缓解帕金森病进展的潜在策略。 Parkinson′s disease(PD)is a common neurodegenerative disorder characterized by progressive loss of dopaminergic neurons of the substantia nigra.While the etiology of PD is likely multifactorial,and the neuroinflammation is a significant component to the pathogenesis of the disease.The nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasomes are multiprotein innate immune complexes regulating inflammation.In the neuroinflammation of PD,the assembly of NLRP3 inflammasome complexes could recruit and activate the caspase-1.Activated caspase-1 cleaves the precursors of interleukin-1βas well as interleukin-18 to produce the downstream inflammatory cascade damaging the dopaminergic neuron.This review provides an overview of the recent studies concerning NLRP3 inflammasome in the pathophysiology of PD,and discusses potential therapeutic strategies to alleviate the progression of PD by inhibiting NLRP3 inflammasome.

关 键 词： 帕金森病 半胱氨酸天冬氨酸蛋白酶 炎症 核苷酸结合寡聚化结构域样受体蛋白

领　　域： []