Abstract：
Although multiple purinergic receptors mediate the analgesic effects of acupuncture, it remains unclear whether there is mutual interaction between purinergic receptors to jointly mediate the electroacupuncture inhibition of peripheral sensitization in visceral pain. Visceral hypersensitivity was induced by intracolonic 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rat. The antinociception effect of electroacupuncture on visceral pain was evaluated by morphology, behaviors, neuroelectrophysiology and molecular biology techniques. After labeling the colon-related primary sensory neurons with neural retrograde tracer and employing neuropharmacology, neuroelectrophysiology, and molecular biotechnology, the mechanisms of P2X7R, P2Y1R, and P2X3R in colon-related dorsal root ganglion (DRG) neurons alleviating visceral hypersensitivity of irritable bowel syndrome (IBS) by electroacupuncture at Zusanli and Sanyinjiao acupoints.were elucidated from the perspective of peripheral sensitization. Electroacupuncture significantly inhibited TNBS-induced colonic hypersensitivity in rats with IBS, and Satellite Glial Cells (SGCs) in DRG were found to be involved in electroacupuncture-mediated regulation of the electrophysiological properties of neurons. P2X7R was found to play a pain-inducing role in IBS visceral hypersensitivity by affecting P2X3R, and electroacupuncture exerted an analgesic effect by inhibiting P2X7R activation. P2Y1R was found to play an analgesic role in the process of visceral pain, mediating electroacupuncture to relieve visceral hypersensitivity. P2Y1R relieved visceral pain by inhibiting P2X3R in neurons associated with nociception, with P2X7R identified as upstream of P2Y1R up-regulation by electroacupuncture. Our study suggests that the P2X7R → P2Y1R → P2X3R inhibitory pathway in DRG mediates the inhibition of peripheral sensitization by electroacupuncture in rats with IBS visceral hypersensitivity.
摘要：
尽管多个嘌呤能受体介导针灸的镇痛作用，目前尚不清楚嘌呤受体之间是否存在相互作用，共同介导电针抑制内脏痛的外周致敏作用。结肠内2,4,6-三硝基苯磺酸（TNBS）在大鼠中诱导内脏超敏反应。通过形态学评价电针对内脏痛的镇痛作用,行为,神经电生理学和分子生物学技术。在用神经逆行示踪剂标记结肠相关的初级感觉神经元并采用神经药理学后，神经电生理学，和分子生物技术，P2X7R的机制，P2Y1R,结肠相关背根神经节（DRG）神经元中的P2X3R通过电针足三里和三阴交穴减轻肠易激综合征（IBS）的内脏高敏感性。从外周敏化的角度进行了阐述。电针显著抑制TNBS诱导的IBS大鼠结肠超敏反应,发现DRG中的卫星胶质细胞（SGC）参与电针介导的神经元电生理特性的调节。发现P2X7R通过影响P2X3R在IBS内脏超敏反应中起疼痛诱导作用，电针通过抑制P2X7R激活而发挥镇痛作用。发现P2Y1R在内脏痛的过程中起镇痛作用，介导电针缓解内脏高敏感性。P2Y1R通过抑制与伤害性感受相关的神经元中的P2X3R缓解内脏痛，P2X7R被确定为通过电针上调P2Y1R的上游。我们的研究表明，DRG中的P2X7R→P2Y1R→P2X3R抑制途径介导了电针对IBS内脏高敏感性大鼠外周致敏的抑制。
