Toll-like receptor 2 plays an essential role in electroacupuncture analgesia in a mouse model of inflammatory pain

• Published in: Acupuncture in medicine : journal of the British Medical Acupuncture Society Vol. 37; no. 6; pp. 356 - 364
• Main Authors: Hsu, Hsin-Cheng, Hsieh, Ching-Liang, Wu, Shu-Yih, Lin, Yi-Wen
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.12.2019; Sage Publications Ltd
• Subjects: Acupuncture; Acupuncture Analgesia; Animals; Cytokines; Disease Models, Animal; Electroacupuncture; Humans; Hyperalgesia; Hyperalgesia - genetics; Hyperalgesia - immunology; Hyperalgesia - therapy; Inflammation; Male; Mice; Mice, Inbred C57BL; Pain; Pain Management; Rodents; Toll-Like Receptor 2 - genetics; Toll-Like Receptor 2 - immunology; pain management; electroacupuncture; chemokines; pro-inflammatory cytokines; toll-like receptor 2
• ISSN: 0964-5284; 1759-9873
• DOI: 10.1136/acupmed-2017-011469

Background: Inflammatory pain occurs when local tissue injury activates macrophages and neutrophils, hence increasing pro-inflammatory cytokine and chemokine levels. Toll-like receptor 2 (TLR2) antagonism reportedly suppresses neuropathic and inflammatory pain. Aims: In the present study, we investigated the effect of electroacupuncture (EA) on TLR2 and related signalling molecules in a complete Freund’s adjuvant (CFA)-induced mouse model of inflammatory pain to determine whether EA can attenuate inflammatory pain via the TLR2 signalling pathway. Methods: EA significantly reduced mechanical and thermal hyperalgesia in the animal model. A similar effect was produced by TLR2 antagonism induced by CU-CPT22 injection. Results: TLR2 expression in the dorsal root ganglia, spinal cord and thalamus increased following induction of inflammation. Expression levels of downstream molecules such as pPI3K, pAkt and pmTOR also increased, as did those of MAPK subfamily members such as pERK, pp38 and pJNK. Transcription factors (pCREB and pNFκB) and nociceptive ion channels (Nav1.7 and Nav1.8) were also involved. Conclusion: Increased expression of the above molecules was attenuated by both EA and TLR2 antagonism. Our results show that EA attenuates inflammatory pain via TLR2 signalling.