炎症体
小胶质细胞
医学
牙髓炎
神经病理性疼痛
促炎细胞因子
牙本质小管
牙痛
TLR4型
药理学
背根神经节
炎症
内科学
病理
牙髓(牙)
解剖
牙本质
牙科
背
作者
Shiren Sun,Wenkai Jiang,Yan Xia,Jing Zhang,Lei Gao,Chunfeng Wu,Bin Zhu,Li‐an Wu
标识
DOI:10.1016/j.brainresbull.2022.10.020
摘要
Emerging research has revealed that the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasomes contribute to the development of inflammatory and neuropathic pains. In addition, microglia are involved in the central nervous system (CNS) pain conduction. However, the relationship between NLRP3 inflammasome and dental inflammatory pain conduction is yet to be established. Therefore, this study aimed to investigate the roles of P2X7 and NLRP3/Caspase-1 (CASP1) in the inflammatory pain caused by pulpitis using a rat experimental pulpitis model. We discovered that the decreased pain threshold was inversely correlated with the increased expression of NLRP3, Caspase-1, P2X7, interleukin-1β (IL-1β), and IL-18 in the trigeminal ganglion and dorsal horn of the medulla after dental pulp exposure. Furthermore, the pain threshold of rats caused by pulpitis was increased by intraperitoneal injection of Brilliant Blue G (BBG), a P2X7 inhibitor, and the expression levels of NLRP3 and related inflammatory factors IL-1β and IL-18 were decreased. Moreover, treatment with 130 nM KCl, a P2X7 inhibitor, significantly reduced the expression of NLRP3, IL-1β, IL-18, Caspase-1, and P2X7 in microglia after lipopolysaccharide(LPS) stimulation. In conclusion, our findings suggest that NLRP3/ CASP1 plays a vital role in the conduction of dental pain; the P2X7regulates NLRP3 pathway in the context of dental inflammatory pain conduction, and inhibiting P2X7 may be a potential strategy for dental inflammatory pain relief.
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