Acupuncture is an emerging alternative therapy that has been beneficial for the pain of osteoarthritis (OA). However, the underlying mechanism of protective effect remains unclear. MCP1/CCR2 axis can be stimulated in various periods of OA, and we hypothesize that acupuncture may treat OA by regulating the MCP1/CCR2 axis. This study aimed to explore the effect of acupuncture at points ST35 and ST36 on the effects of hyperalgesia and cartilage in OA rats including the expression of chemokines, nerve growth factor (NGF), and inflammatory-related proteins. OA was induced in male Sprague–Dawley rats by anterior cruciate ligament transection at the right knee. The first acupuncture intervention was performed on the seventh day after surgery and once a day for seven weeks. The knee-pain-related behaviors, histology, and related protein were examined in this study. We have found that electroacupuncture at ST35 and ST36 can significantly alleviate the hyperalgesia and cartilage degeneration as well as reducing nerve sprouting in OA knee joint. Moreover, acupuncture treatment may inhibit the MCP1/CCR2 axis as well as down-regulate inflaming factor and NGF in cartilage and synovial tissue. The data presented here indicate that acupuncture exerts a protective effect against hyperalgesia and cartilage degeneration, and the mechanism might involve in chemokines and NGF pathway.

Impact statement

Osteoarthritis (OA) is the most common form of arthritis, affecting an estimated 302 million people worldwide, but the mechanism of OA is far away understood. Acupuncture has been widely used in treating with chronic pain, but how does acupuncture work is still unclear. In this essay, we investigated the molecular target of acupuncture and found new mechanism of the pathogenesis in knee OA. Our results could provide new analgesic mechanisms and find new targets for acupuncture analgesia in OA. In a word, the study can help further understanding and provides more evidence of the clinical use of acupuncture in treating OA.

中文翻译：

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针灸通过抑制 MCP2/CCR2 信号通路减轻骨关节炎大鼠的疼痛。

针灸是一种新兴的替代疗法，对骨关节炎 (OA) 的疼痛有益。然而，保护作用的潜在机制尚不清楚。MCP1/CCR2轴可以在OA的不同时期受到刺激，我们假设针灸可能通过调节MCP1/CCR2轴来治疗OA。本研究旨在探讨针刺 ST35 和 ST36 穴对 OA 大鼠痛觉过敏和软骨的影响，包括趋化因子、神经生长因子 (NGF) 和炎症相关蛋白的表达。通过右膝前交叉韧带横断在雄性 Sprague-Dawley 大鼠中诱导 OA。第一次针灸干预在术后第七天进行，每天一次，持续七周。膝痛相关行为、组织学、本研究对相关蛋白进行了检测。我们发现电针 ST35 和 ST36 可以显着减轻痛觉过敏和软骨退变，并减少 OA 膝关节的神经发芽。此外，针灸治疗可能会抑制 MCP1/CCR2 轴以及下调软骨和滑膜组织中的炎症因子和 NGF。这里提供的数据表明，针灸对痛觉过敏和软骨退变具有保护作用，其机制可能涉及趋化因子和 NGF 通路。针刺治疗可能抑制MCP1/CCR2轴，下调软骨和滑膜组织中的炎症因子和NGF。这里提供的数据表明，针灸对痛觉过敏和软骨退变具有保护作用，其机制可能涉及趋化因子和 NGF 通路。针刺治疗可能抑制MCP1/CCR2轴，下调软骨和滑膜组织中的炎症因子和NGF。这里提供的数据表明，针灸对痛觉过敏和软骨退变具有保护作用，其机制可能涉及趋化因子和 NGF 通路。

影响陈述

骨关节炎 (OA) 是最常见的关节炎形式，影响全球约 3.02 亿人，但对 OA 的机制尚不清楚。针灸已被广泛用于治疗慢性疼痛，但针灸如何起作用尚不清楚。在本文中，我们研究了针灸的分子靶点，并发现了膝关节 OA 发病机制的新机制。我们的研究结果可以提供新的镇痛机制，并为针刺镇痛 OA 找到新的靶点。总之，该研究有助于进一步了解针灸治疗OA的临床应用并提供更多证据。