三叉神经节中的 P2Y 受体有助于维持炎症性疼痛。
The P2Y receptor in the trigeminal ganglion contributes to the maintenance of inflammatory pain.
机构信息
State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
Laboratory of Anesthesia & Critical Care Medicine, Translational Neuroscience Center, West China Hospital of Sichuan University, Chengdu, 610041, China.
出版信息
Neurochem Int. 2019 Dec;131:104567. doi: 10.1016/j.neuint.2019.104567. Epub 2019 Oct 3.
P2Y purinergic receptors expressed in neurons and satellite glial cells (SGCs) of the trigeminal ganglion (TG) contribute to inflammatory and neuropathic pain. P2Y receptor expression is reported in the spinal cord, dorsal root ganglion (DRG), and TG. In present study, the role of P2Y receptor in the TG in inflammatory orofacial pain of Sprague-Dawley (SD) rats was investigated. Peripheral injection of complete Freund's adjuvant (CFA) induced mechanical hyperalgesia with the rapid upregulation of P2Y receptor, glial fibrillary acidic protein (GFAP), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), C-C chemokine CCL2, phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated p38 (p-p38) proteins in the TG. Furthermore, immunofluorescence staining confirmed the CFA-induced upregulation of P2Y receptor. Double immunostaining showed that P2Y receptor colocalized with glutamine synthetase (GS) and neuronal nuclei (NeuN). Finally, trigeminal injection of a selective antagonist (PPTN) of P2Y receptor attenuated CFA-induced mechanical hyperalgesia. PPTN also decreased the upregulation of the GFAP, IL-1β, TNF-α, CCL2, p-ERK1/2, and p-p38 proteins. Our findings showed that P2Y receptor in TG may contribute to orofacial inflammatory pain via regulating SGCs activation, releasing cytokines (IL-1β, TNF-α, and CCL2), and phosphorylating ERK1/2 and p38.
P2Y 嘌呤能受体在三叉神经节（TG）中的神经元和卫星神经胶质细胞（SGC）中表达，有助于炎症性和神经性疼痛。据报道，P2Y 受体在脊髓、背根神经节（DRG）和 TG 中表达。在本研究中，研究了 P2Y 受体在 Sprague-Dawley（SD）大鼠炎症性口腔面部疼痛中的 TG 中的作用。完全弗氏佐剂（CFA）的外周注射引起机械性痛觉过敏，伴随着 P2Y 受体、胶质纤维酸性蛋白（GFAP）、白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）、C-C 趋化因子 CCL2、磷酸化细胞外信号调节激酶 1/2（p-ERK1/2）和磷酸化 p38（p-p38）蛋白在 TG 中的快速上调。此外，免疫荧光染色证实了 CFA 诱导的 P2Y 受体上调。双重免疫染色显示 P2Y 受体与谷氨酰胺合成酶（GS）和神经元核（NeuN）共定位。最后，三叉神经注射 P2Y 受体的选择性拮抗剂（PPTN）减弱了 CFA 诱导的机械性痛觉过敏。PPTN 还降低了 GFAP、IL-1β、TNF-α、CCL2、p-ERK1/2 和 p-p38 蛋白的上调。我们的研究结果表明，TG 中的 P2Y 受体可能通过调节 SGCs 激活、释放细胞因子（IL-1β、TNF-α 和 CCL2）以及磷酸化 ERK1/2 和 p38 来促进口腔炎症性疼痛。
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