Acupuncture, Inflammation, and the Motor System

In the motor system, inflammatory conditions such as osteoarthritis (OA), muscle strain, and tendon injury are very common and respond well to acupuncture in clinical practice. OA is characterized by joint pain, swelling, stiffness, synovial inflammation, articular cartilage damage, and reduced bone density around the joint.

In OA, infiltrating inflammatory cells release cytokines and chemokines that drive and maintain the disease. T and B lymphocytes, synovial macrophages, and synovial fibroblasts accumulate in the locally inflamed synovium. Pro-inflammatory mediators such as IL-1β, TNF-α, IL-6, and MMP-1, MMP-3, MMP-13 promote synovial hyperplasia and fibrosis, erode cartilage, and eventually disrupt the mechanical balance of the joint.

A growing number of studies show that acupuncture can effectively alleviate inflammation in the motor system. Below is a summary of the mechanisms, focusing on monocytes/macrophages, matrix metalloproteinases (MMPs), and key signaling pathways in joints, tendons, and muscles.

1. Monocytes/Macrophages and Synovial Inflammation

In articular cartilage, synovial membrane, and synovial fluid, monocytes and macrophages can be activated by the chemokine MCP-1. Once activated, they release matrix-degrading enzymes, maintain leukocyte infiltration, and trigger synovial reactions and joint destruction.

Several animal studies have demonstrated that acupuncture at specific acupoints can modulate this pathway:

• MA at Dubi (ST35) and ST36 Inhibits MCP-1 and its receptor CCR2 in synovium and cartilage, down-regulates IL-1β and TNF-α in joint tissue, and protects cartilage and synovium from inflammatory damage.
• EA at Neixiyan (Ex-LE4) and ST35 Down-regulates IKK-β and NF-κB p65, up-regulates IκB-α in chondrocytes, inhibits IL-1β, IL-6, TNF-α in cartilage and synovial fluid, and delays cartilage degeneration in OA models.
• EA at ST36 and GB34 Inhibits TLR4, NF-κB p65, and NF-κB p-p65 in articular cartilage and exerts anti-inflammatory effects in OA. The combined use of ST36 + GB34 is superior to GB34 alone, highlighting the benefit of multi-point treatment.

One study used post-acupuncture serum (EAS) as an intervention. Serum collected after EA was applied to TNF-α–treated chondrocytes and was found to:

• Significantly reduce IL-1β levels
• Enhance chondrocyte viability
• Inhibit RAS, RAF, MEK1/2, and p-ERK1/2 protein expression

This concept of “acupuncture serum” suggests a potential direction for transforming acupuncture signals into biological agents or “acupuncture-inspired drugs”.

EA at Ex-LE4 and ST35 also inhibits activation of the NLRP3 inflammasome in cartilage tissue of OA rats, reduces downstream inflammatory mediators such as IL-1β and the converting enzyme caspase-1, and alleviates local inflammatory responses.

2. Tendon Repair and Muscle Protection

Acupuncture also shows important benefits in tendon injury and muscle atrophy.

In an Achilles tendon injury model:

• MA combined with EA at ST36, Chengshan (BL57), and ST36+BL57 reduces inflammation and promotes early remodeling of the tendon.
• Increases non-collagen components within the Achilles tendon, enhances tendon strength, and shortens the early-stage tendon repair period.

For denervation-induced muscle atrophy:

• Acupuncture with low-frequency electrical stimulation (Acu-LFES) at GB34 and ST36 attenuates muscle atrophy caused by nerve injury.
• Stimulates the expression of macrophages and IL-6 in both normal and denervated muscle and in serum.
• Up-regulates the IGF-1/Akt signaling pathway, preventing loss of soleus and plantaris muscle weight and helping maintain muscle volume.

3. MMPs, Synovial Chemokines, and the Gut–Joint Axis

In OA, matrix metalloproteinases (MMPs) derived from synovial macrophages and fibroblasts destroy the extracellular matrix and aggravate inflammatory cell infiltration.

Studies show that:

• EA at ST36 and GB34 significantly reduces MIP-1α, MIP-2, and MCP-1 in serum and synovial fluid, inhibits MMP expression, and down-regulates inflammatory mediators such as VEGF, IP-10, IL-1α, TNF-α, and leptin, thereby suppressing LPS-mediated arthritis in obese rats.
• EA modulates intestinal microbiota by increasing the Bacteroidetes/Firmicutes ratio and restoring the abundance of Clostridium, Akkermansia, Butyricimonas, and Lactococcus, suggesting a gut–joint axis in acupuncture’s anti-inflammatory effects.
• EA at ST35 and Ex-LE4 reduces MMP-3 and MMP-13 expression in chondrocytes, regulates cartilage matrix metabolism, decreases degradation of type II collagen, and relieves knee arthritis.

4. Clinical Insights: Beyond Pain Relief

Overall, these studies suggest that acupuncture in motor system disorders:

• Down-regulates chemokines such as MCP-1, MIP-1α, MIP-2 and key cytokines including IL-1β, IL-6, TNF-α.
• Inhibits NF-κB, TLR4, NLRP3 and related inflammatory pathways in synovium and cartilage.
• Protects articular cartilage, reduces synovial hyperplasia and fibrosis, and supports tendon remodeling and muscle preservation.
• Exerts systemic effects through modulation of the intestinal microbiota, suggesting a gut–immune–joint axis.

In practice, combinations such as ST35 + Ex-LE4, ST36 + GB34, ST36 + BL57, GB34 + ST36 are often more effective than single points alone, providing not just analgesia but also biological modulation of inflammation and tissue repair.

在運動系統相關疾病中，退化性關節炎（osteoarthritis, OA）、肌肉拉傷、 肌腱損傷，是臨床上非常常見且對針灸反應良好的一群疾病。OA 患者常見 關節疼痛、腫脹、僵硬，並伴隨滑膜發炎、關節軟骨破壞以及關節周圍 骨質密度下降。

在 OA 的病程中，浸潤至滑膜與關節腔內的發炎細胞會釋放各種 細胞激素（cytokines）與趨化因子（chemokines）。包括 T 細胞、B 細胞、滑膜巨噬細胞、滑膜成纖維細胞等浸潤於病變滑膜，並分泌 IL-1β、TNF-α、IL-6 以及 MMP-1、MMP-3、MMP-13 等基質金屬蛋白酶， 造成滑膜增生與纖維化，逐步侵蝕關節軟骨，破壞關節受力平衡。

越來越多研究指出，針灸可以有效減輕運動系統的發炎反應。以下從單核球／巨噬細胞、 MMP 以及主要訊號通路出發，整理關節、肌腱與肌肉層面的相關機制。

一、單核球／巨噬細胞與滑膜發炎

在關節軟骨、滑膜與滑液中，單核球／巨噬細胞會受到趨化因子 MCP-1 的活化，進而釋放各種基質降解酶，驅動並維持白血球浸潤，引發滑膜反應 與關節破壞。

動物實驗顯示，針灸於特定穴位可以調節這個惡性循環：

• 針刺 犢鼻（ST35）、足三里（ST36） 抑制滑膜與軟骨組織中的 MCP-1 及其受體 CCR2，下調關節組織內 IL-1β、TNF-α，保護關節軟骨與滑膜免於發炎性損傷。
• 電針 內膝眼（Neixiyan, Ex-LE4）、犢鼻（ST35） 下調軟骨細胞中的 IKK-β、NF-κB p65，上調 IκB-α，抑制關節軟骨與 滑液中的 IL-1β、IL-6、TNF-α，延緩退化性關節炎模型中的軟骨退變。
• 電針 足三里（ST36）、陽陵泉（GB34） 抑制關節軟骨中的 TLR4、NF-κB p65、NF-κB p-p65，發揮抗發炎效果；且 ST36+GB34 雙穴合用 優於單刺陽陵泉，凸顯「配穴」的重要性。

有研究進一步採用「針後血清（EAS, electroacupuncture serum）」概念： 先對動物施以電針，再取其血清，加入接受 TNF-α 處理的軟骨細胞培養中，結果發現：

• IL-1β 顯著下降
• 軟骨細胞存活率提高
• RAS、RAF、MEK1/2、p-ERK1/2 蛋白表現被抑制

這種以「針灸後血清」作為介入的方式，提出了一個有趣的方向：未來是否可以將針灸刺激所誘發的 體液變化，發展成類似「針灸藥物」或生物製劑，是值得持續探討的議題。

在 OA 大鼠模型中，電針 內膝眼（Ex-LE4）、犢鼻（ST35） 亦可抑制關節軟骨組織中 NLRP3 發炎小體的活化，下調下游 IL-1β 及其轉化酶 caspase-1，進一步緩解局部發炎反應。

二、肌腱修復與肌肉萎縮保護

針灸的作用不僅限於關節腔結構，對肌腱修復與肌肉保護也有重要意義。

在阿基里斯腱損傷模型中：

• 針刺結合電針 足三里（ST36）、承山（BL57）及 ST36+BL57 組合 能減少局部發炎，促進早期組織重塑。
• 增加阿基里斯腱中的非膠原成分，提高肌腱強度，縮短早期肌腱修復期。

在去神經支配（denervation）導致的肌肉萎縮模型中：

• 陽陵泉（GB34）、足三里（ST36）之低頻電刺激（Acu-LFES） 可減輕去神經所造成的肌肉萎縮。
• 提高正常及去神經肌肉及血清中巨噬細胞與 IL-6 的表現。
• 上調 IGF-1／Akt 訊號通路，預防比目魚肌與撓側肌重量下降，有助於維持 肌肉體積。

三、MMP、滑膜趨化因子與腸道－關節軸

在 OA 病程中，滑膜巨噬細胞與成纖維細胞所分泌的 基質金屬蛋白酶（MMPs） 會破壞細胞外基質，並加劇發炎細胞浸潤。

文獻指出：

• 電針 足三里（ST36）、陽陵泉（GB34） 可明顯降低血清與滑液中的 MIP-1α、MIP-2、MCP-1，抑制 MMPs 表現，並下調 VEGF、IP-10、IL-1α、TNF-α、leptin 等發炎與代謝相關介質，在肥胖大鼠的 LPS 介導性關節炎模型中具有明顯的抑制關節發炎效果。
• 電針同時調整腸道菌相，提高 Bacteroidetes／Firmicutes 比值， 恢復 Clostridium、Akkermansia、Butyricimonas、Lactococcus 等菌屬的相對 豐度，顯示出「腸道－免疫－關節軸」在針灸抗發炎作用中的潛在角色。
• 電針 犢鼻（ST35）、內膝眼（Ex-LE4） 降低軟骨細胞中的 MMP-3、MMP-13，調節軟骨基質代謝，減少第二型膠原 （type II collagen）分解，緩解膝關節炎並保護關節結構。

四、小結：不只是止痛，更是調節發炎與修復

綜合這些研究，針灸在運動系統疾病中的作用可以從多個層面來理解：

• 下調 MCP-1、MIP-1α、MIP-2 等趨化因子及 IL-1β、IL-6、TNF-α 等關鍵發炎細胞激素。
• 抑制 NF-κB、TLR4、NLRP3 等發炎訊號通路，減少滑膜與軟骨炎性破壞。
• 保護關節軟骨，減少滑膜增生與纖維化，並促進肌腱重塑與肌肉保留。
• 經由腸道菌相調整，從「腸道－免疫－關節」軸向，提供更全面的抗發炎效果。

在臨床實務上，像是 ST35+Ex-LE4、ST36+GB34、ST36+BL57、GB34+ST36 等配穴， 常不僅止於「止痛」，也能在病程中提供發炎調節與組織修復支持。