前动力蛋白2介导躯体疼痛的外周与中枢神经敏化

前动力蛋白2(prokineticin 2，PK2) 是新近发现的一种趋化因子，通过与受体PKR1和PKR2结合，参与机体多种生理功能。PK信号通路是近年来新发现的组织损伤和神经损伤后疼痛发生和维持的重要调节通路，其在调节伤害性事件方面起着关键作用，是众多疾病的潜在治疗靶点。PKRs的激活可以引起痛觉感受，参与痛觉感受器对不同刺激的敏感性。PK系统（PKs和PKRs）是在免疫细胞中参与炎症发生和疼痛传递的重要环节。PK2通过激活初级传入神经元上的PKR1和PKR2参与调节痛觉感知，在大鼠初级感觉神经元中，PK2还通过PKC信号通路增强门控离子通道电流，抑制γ-氨基丁酸(GABA)激活电流，敏化嘌呤核苷酸P2受体(P2X)。本文围绕PK2在躯体疼痛中的研究进展进行述评，以期在未来的研究中，有望找到以PK信号通路为靶点的炎性疼痛治疗的新药。

Prokineticin 2 mediates peripheral and central sensitization of somatic pain

Prokineticin 2 (PK2) is a newly discovered chemokine, which participates in various physiological functions of the body by binding to receptors PKR1 and PKR2. PK signaling pathway is a newly discovered important regulatory pathway for the occurrence and maintenance of pain after tissue injury and nerve injury in recent years. It plays a key role in regulating injury-related nociceptive events and is a potential therapeutic target for many diseases. The activation of PKRs can induce pain sensation and participate in the sensitivity of pain receptors to different stimuli. The PK system (PKs and PKRs) is an important link involved in inflammation and pain transmission in immune cells. PK2 is involved in the regulation of pain perception by activating PKR1 and PKR2 on primary sensory neurons. In rat primary sensory neurons, PK2 also enhances gated ion channel current through the PKC signaling pathway, inhibits GABA-activated currents, and sensitizes purine nucleotide P2 receptor (P2X). This paper reviews the research progress of PK2 in physical pain. We hope to find new drugs for the treatment of inflammatory pain that target the PKs signaling pathway in future studies.