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Acupuncture in medicine : journal of the British Medical Acupuncture Society · 2026

Anti-inflammatory mechanisms underlying sympathetic nervous system-mediated acupuncture analgesia.

СтатьяНазвание и аннотация: Перевод в очереди
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Zhou Dao-Peng, Teng Jin-Yan, Wang Jie-Yu, Zheng Yi-Wei

Аннотация

Sympathetic nerves play an important role in the generation and maintenance of pain, and many studies have shown that inflammatory factors play an important role in this process. During tissue inflammation or injury, the interaction between sympathetic nerves and the sensory nervous system may lead to the aggravation of pain. Inflammatory mediators such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β play a key role in soft tissue injury and complex regional pain syndrome (CRPS) and thus affect the perception and regulation of pain through sympathetic nerve pathways. The efficacy of acupuncture and moxibustion in the treatment of pain disorders has been verified in clinical practice, and significant results have been achieved. As an exogenous nerve stimulation technique, acupuncture can stimulate a variety of anti-inflammatory pathways mediated by sympathetic nerves, to regulate the activity of sympathetic nerves and the release of neurotransmitters, regulate inflammatory cytokines and signaling pathways, and interfere with nerve-immune interaction, thus inducing anti-inflammatory and analgesic effects. In conclusion, acupuncture treatment has shown positive effects in the management of pain caused by sympathetic nerves and soft tissues, and the mechanism may involve the regulation of the nervous system mediated by the modulation of inflammatory factors. These findings provide a scientific basis for the use of acupuncture in pain management and, although the underlying mechanisms remain unclear, suggest new directions for future research. This article explores the pathways underlying acupuncture analgesia and specifically examines the role of sympathetic nerves.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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