慢性炎症痛是常见慢性痛，其持续时间较长，严重影响患者生活质量，往往给患者带来沉重身心负担。针刺是一种可有效缓解慢性痛的治疗手段，然而其镇痛机制目前尚不完全清楚。近期研究发现针刺的镇痛机制可能与其干预和调节中枢或外周与痛觉或炎症相关的分子或信号通路有关。有证据表明趋化因子CCL3信号通路参与了慢性痛。本项目拟通过观察慢性炎症痛对外周感觉神经元CCL3通路表达的调控作用，探讨外周CCL3通路参与慢性炎症痛的分子机制，进而确立该通路在慢性炎症痛中的重要作用。在此基础上，利用免疫印记、神经电生理、细胞内钙成像、药理学等手段探讨慢性炎症痛情况下电针对CCL3通路表达和功能的干预作用以及该通路在电针镇痛效应中的参与机制。本项目的开展将有助于进一步揭示慢性炎症痛产生的分子机制，同时为针刺镇痛效应的机制研究提供崭新理论依据，从而更好地指导针刺镇痛的临床实践工作。

Chronic inflammatory pain is a common form of chronic pain. It has long duration and severely affects the normal life of the patients. Acupuncture is an efficient therapy to alleviate chronic pain. However, the mechanisms of acupuncture analgesia are still not fully understood. Recent studies suggest that acupuncture analgesia may be due to the intervention of acupuncture in peripheral or central pain/inflammatory molecule or signaling pathway. Evidence has suggested that chemokine CCL3 signaling is involved in chronic pain. Therefore, this current project aims to establish a pivotal role of CCL3 signaling of primary sensory neurons in chronic inflammatory pain by investigating the regulatory effects of chronic inflammatory pain on CCL3 signaling and the molecular mechanisms underlying the involvement of CCL3 signaling in chronic inflammatory pain. Next, we aim to explore the intervention of electroacupuncture (EA) on CCL3 signaling in the context of chronic inflammatory pain and the involvement of CCL3 signaling in EA induced analgesia by means of immunoblotting, electrophysiology, calcium imaging and pharmacology. This project will further unravel the molecular mechanisms of chronic inflammatory pain and provide novel theory for the explanation of acupuncture analgesia, which may help to improve the clinical practice of acupuncture analgesia.