Acupuncture points injection mitigates chronic pain through transient receptor potential V1 in mice

被引:1
|
作者
Liao, Hsien-Yin [1 ]
Lin, Ming-Chia [2 ]
Lin, Yi-Wen [3 ,4 ]
机构
[1] China Med Univ, Sch Postbaccalaureate Chinese Med, Coll Chinese Med, Taichung 40402, Taiwan
[2] I Shou Univ, E DA Hosp, Dept Nucl Med, Coll Med, Kaohsiung 82445, Taiwan
[3] China Med Univ, Grad Inst Acupuncture Sci, Coll Chinese Med, 91 Hsueh Shih Rd, Taichung 404, Taiwan
[4] China Med Univ, Chinese Med Res Ctr, Taichung 40402, Taiwan
关键词
Acupuncture points; injection; Chronic inflammatory; pain; Dorsal root ganglion; Iba1; Somatosensory cortex; TRPV1; TRPV1; PROLOTHERAPY; HYPERALGESIA; MODULATION; NEURONS; SYSTEM;
D O I
10.22038/IJBMS.2022.60121.13327
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective(s): Tissue injury in peripheral sites can result in long-term potentiation in nociceptive neurons and surrounding glial cells, potentially resulting in the development of chronic inflammatory pain (CIP). Acupoint injection (AI) is similar to Western phototherapy, which injects solutions at specific sites to mitigate chronic pain. AI has shown greater benefits compared with acupuncture. In this study, we examined the therapeutic effect and explored the underlying mechanisms of AI in mice CIP model. Materials and Methods: We injected thrice complete Freund???s adjuvant (CFA) into the mouse???s hind paw to induce CIP. Results: We found that, after two weeks, CFA injection significantly induced mechanical and thermal hyperalgesia which were attenuated by AI treatment. Transient receptor potential V1 (TRPV1) channels and associated molecules were all increased in CIP in mice dorsal root ganglion (DRG), spinal cord (SC), thalamus, and somatosensory cortex (SSC). The aforementioned molecules were mitigated in AI and Trpv1 knockout mice. Furthermore, Iba1-positive cells (microglial marker) were also potentiated and shared a similar tendency with TRPV1. Conclusion: These findings suggest that AI can alleviate chronic pain by reducing TRPV1 overexpression in both neuronal and microglial cells. Our results suggest new potential therapeutic targets for AI in chronic pain.
引用
收藏
页码:451 / 459
页数:9
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