Acupoint catgut embedding attenuates fibromyalgia pain through attenuation of TRPV1 signaling pathway in mouse.

Fibromyalgia causes widespread chronic pain lasting more than three months, along with anxiety, sleep problems, and depression. Researchers studied a specialized acupuncture technique called acupoint catgut embedding (ACE) to see if it could help relieve fibromyalgia pain in mice. This technique involves embedding small pieces of catgut (absorbable surgical thread) at acupuncture points, which provides continuous stimulation over time rather than requiring frequent visits. The study focused on a specific pain receptor in the body called TRPV1, which transmits pain and inflammation signals to the brain. Researchers induced fibromyalgia-like symptoms in mice using cold stress, then treated them with ACE at the ST36 acupoint (located on the lower leg). The results showed significant pain reduction in mice receiving ACE treatment. Mechanical pain sensitivity improved from 1.85g to 3.99g, and thermal pain sensitivity improved from 4.85 seconds to 7.42 seconds by day 14. The treatment also reduced inflammatory chemicals in the body and decreased TRPV1 activity in pain-processing areas of the brain, including the thalamus and cortex regions. Mice genetically modified to lack TRPV1 receptors showed similar pain improvements, suggesting that blocking this receptor is key to ACE's pain-relieving effects. This research indicates that acupoint catgut embedding may offer a promising treatment option for fibromyalgia patients by targeting specific pain pathways in the nervous system. If considering acupuncture for fibromyalgia, seek treatment from a licensed acupuncturist trained in specialized techniques.

This preclinical study investigated acupoint catgut embedding (ACE) for fibromyalgia pain management through TRPV1 pathway modulation. Researchers induced FM in mice via cold stress and administered bilateral ACE at ST36. By day 14, ACE-treated mice demonstrated significant analgesia compared to FM controls: mechanical threshold increased from 1.85±0.13g to 3.99±0.16g, and thermal latency improved from 4.85±0.26s to 7.42±0.45s. Trpv1-/- knockout mice showed comparable improvements (mechanical: 4.25±0.2g; thermal: 7.91±0.21s), confirming TRPV1's mechanistic role. ACE treatment reduced inflammatory mediators and downregulated TRPV1 expression in key pain-processing centers including the thalamus, somatosensory cortex, medial prefrontal cortex, and anterior cingulate cortex. Results were comparable between ACE intervention and genetic TRPV1 ablation, suggesting ACE exerts analgesic effects through TRPV1 pathway inhibition. Clinical implications support ACE as a potential therapeutic approach for FM management, offering sustained stimulation with reduced treatment frequency compared to traditional acupuncture.