NLRP3炎症小体在辐射损伤中的研究进展

Research Progress of NLRP3 Inflammasome in Radiation Damage

NLRP3是核苷酸结合寡聚结构域(NOD)样受体(NLR)的一员,是由NOD、LRR和pyrin结构域组成的一种多蛋白复合物,其导致caspase-1的自身蛋白水解激活,随后引发促炎细胞因子IL-1β和IL-18释放,导致细胞焦亡。放射疗法(RT)是恶性肿瘤的主要治疗方式之一,但其引起的损伤极大影响着患者的预后,极大限制RT的应用。因此探寻辐射损伤的有效防护及缓解方式迫在眉睫。有研究指出NLRP3炎症小体在辐射损伤中发挥着重要作用,并已有大量研究探讨NLRP3在辐射所造成损伤产生的作用及其机制。本文将阐述NLRP3炎症小体对辐射引起多种损伤的影响及其激活机制,以寻找预防或抵抗辐射损伤的潜在作用路径。

NLRP3 is a member of nucleotide binding oligomeric domain (NOD)-like receptors (NLR), a mul-ti-protein complex composed of NOD, LRR, and pyrin domains, which leads to autoproteolytic ac-tivation of caspase-1, followed by the release of pro-inflammatory cytokines IL-1β and IL-18, leading to pyrosis. Radiation therapy (RT) is one of the main treatment modalities for malignant tumors, but the damage caused by it greatly affects the prognosis of patients and greatly limits the use of RT. Therefore, it is urgent to explore effective protection and mitigation methods for radiation damage. Studies have pointed out that NLRP3 inflammasomes play an important role in radiation damage, and a large number of studies have explored the role and mechanism of NLRP3 in radia-tion-induced damage. This article will describe the effects of NLRP3 inflammasomes on various radiation-induced injuries and their activation mechanisms to find potential pathways to prevent or resist radiation damage.