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已发表论文
电针通过 NGF/TrkA 通路缓解膝骨关节炎所致疼痛及软骨退变
Authors Fu Y, Lin L, Chen W, Shi G, Li HP, Tu JF , Liu CZ
Received 5 September 2025
Accepted for publication 16 December 2025
Published 7 January 2026 Volume 2026:19 560506
DOI https://doi.org/10.2147/JPR.S560506
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Houman Danesh
Yiming Fu,* Lulu Lin,* Wen Chen, Guangxia Shi, Hong-Ping Li, Jian-Feng Tu, Cun-Zhi Liu
International Acupuncture and Moxibustion Innovation Institute, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Jian-Feng Tu; Hong-Ping Li, Email tujianfeng1@126.com; hongping_lin022507@163.com
Introduction: Knee osteoarthritis (KOA) is a chronic degenerative joint disease marked by pain, cartilage degradation, and limited mobility. Existing treatments remain suboptimal due to limited efficacy and adverse effects, highlighting the urgent need for safer, mechanism-based therapies. Electroacupuncture (EA) has demonstrated clinical benefits in KOA, yet its underlying molecular mechanisms remain unclear.
Methods: A KOA rat model was established via intra-articular injection of monosodium iodoacetate (MIA). EA was applied at Dubi (ST35) and Neixiyan (EX-LE5) acupoints. We assessed the effect of EA on nociceptive behavior in rats with KOA using von Frey filament testing, weight-bearing asymmetry measurements, and spontaneous pain assays. Cartilage degeneration was analyzed via toluidine blue staining, while immunofluorescence staining quantified protein expression levels in cartilage and dorsal root ganglia (DRG). Inhibitor and agonist injections were employed to evaluate the specific involvement of the NGF/TrkA pathway in EA-mediated effects.
Results: EA significantly reduced mechanical allodynia (p < 0.001), weight-bearing asymmetry (p < 0.001), spontaneous pain (p < 0.001). EA decreased macroscopic chondropathy score (p < 0.01) and cartilage degeneration score (p < 0.001). EA inhibited MMP13 expression (p < 0.05), suppressed NGF (p < 0.001) and TrkA (p < 0.05) expression, decreased PGP9.5 overexpression (p < 0.05), and downregulated pro-inflammatory cytokines IL-1β (p < 0.01) and TNF-α (p < 0.01). Pharmacological inhibition of NGF/TrkA mimicked EA’s effects, while activation of this pathway counteracted its analgesia. EA selectively downregulated TrkA in CGRP+ (p < 0.01), but not IB4+ (p > 0.05) or NF200+ (p > 0.05) DRG neurons subtypes.
Conclusion: Our results demonstrate that EA alleviates KOA, possibly via inhibiting NGF/TrkA pathway activation in knee joints and reducing TrkA expression in CGRP+ sensory neurons, supporting the therapeutic potential of EA for KOA.
Keywords: osteoarthritis, electroacupuncture, nerve growth factor, pain, cartilage diseases
International Acupuncture and Moxibustion Innovation Institute, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Jian-Feng Tu; Hong-Ping Li, Email tujianfeng1@126.com; hongping_lin022507@163.com
Introduction: Knee osteoarthritis (KOA) is a chronic degenerative joint disease marked by pain, cartilage degradation, and limited mobility. Existing treatments remain suboptimal due to limited efficacy and adverse effects, highlighting the urgent need for safer, mechanism-based therapies. Electroacupuncture (EA) has demonstrated clinical benefits in KOA, yet its underlying molecular mechanisms remain unclear.
Methods: A KOA rat model was established via intra-articular injection of monosodium iodoacetate (MIA). EA was applied at Dubi (ST35) and Neixiyan (EX-LE5) acupoints. We assessed the effect of EA on nociceptive behavior in rats with KOA using von Frey filament testing, weight-bearing asymmetry measurements, and spontaneous pain assays. Cartilage degeneration was analyzed via toluidine blue staining, while immunofluorescence staining quantified protein expression levels in cartilage and dorsal root ganglia (DRG). Inhibitor and agonist injections were employed to evaluate the specific involvement of the NGF/TrkA pathway in EA-mediated effects.
Results: EA significantly reduced mechanical allodynia (p < 0.001), weight-bearing asymmetry (p < 0.001), spontaneous pain (p < 0.001). EA decreased macroscopic chondropathy score (p < 0.01) and cartilage degeneration score (p < 0.001). EA inhibited MMP13 expression (p < 0.05), suppressed NGF (p < 0.001) and TrkA (p < 0.05) expression, decreased PGP9.5 overexpression (p < 0.05), and downregulated pro-inflammatory cytokines IL-1β (p < 0.01) and TNF-α (p < 0.01). Pharmacological inhibition of NGF/TrkA mimicked EA’s effects, while activation of this pathway counteracted its analgesia. EA selectively downregulated TrkA in CGRP+ (p < 0.01), but not IB4+ (p > 0.05) or NF200+ (p > 0.05) DRG neurons subtypes.
Conclusion: Our results demonstrate that EA alleviates KOA, possibly via inhibiting NGF/TrkA pathway activation in knee joints and reducing TrkA expression in CGRP+ sensory neurons, supporting the therapeutic potential of EA for KOA.
Keywords: osteoarthritis, electroacupuncture, nerve growth factor, pain, cartilage diseases