Kristen Sparrow • August 08, 2023
In this research study, the authors used a cold invoked fibromyalgia model in mice. They determined that acupuncture catgut embedding lead to less pain as measured by clinical response in addition to lower inflammatory markers in the brain facilitated by the TRPV1 receptor. They knew that the TRPV1 receptor was key because when the experiment was done on mice with a gene deletion for TRPV1, the acupuncture didn’t work.
Amazing work and a fantastic study on a type of therapy that may have more enduring response than a simple acupuncture treatment. It also elucidates what could be an important mechanism for fibromyalgia and lead to further treatment and understanding.
Background: Chronic pain refers to pain that persists for over three months. Chronic pain may restrict activities of daily living, including work, learning, social life, and can lead to anxiety, depression, and sleep disturbance. Imaging data have demonstrated that central sensitization often occurs in the brain of patients with chronic pain, which arises from imbalanced neurotransmission in the central nervous system. Transient receptor potential vanilloid 1 (TRPV1) is an ion channel to serve as an inflammatory detector in the brain. We aim to determine the properties of acupoint catgut embedding (ACE) on cold stress-induced mice fibromyalgia (FM) and surveyed the character of TRPV1 and linked molecules in chronic FM pain.
Methods: Intermittent cold stress (ICS) was used to induce mice FM model. Mice were subgrouped into normal mice, ICS-induced FM group, FM mice with ACE, and FM in Trpv1-/- group. ACE is a novel acupuncture technique that provides convenience and continuous nerve stimulation that has been reported effective on pain management.
Results: Our behavioral experiments showed similar levels of pain response among all groups before treatment. After ICS, prolonged mechanical and thermal pain was initiated (mechanical threshold: 1.96 ± 0.12 g; thermal latency: 4.86 ± 0.21 s) and were alleviated by ACE treatment and TRPV1 gene deletion. Inflammatory mediators were increased in the plasma of FM mice, while TRPV1 and related kinases were amplified in the hypothalamus and cerebellum. These changes were ameliorated in the ACE-treated and Trpv1-/- groups.
Conclusions: These novel findings suggest that chronic FM pain can be modulated by ACE or TRPV1 gene deletion. The analgesic effect of ACE through the TRPV1 pathway may reflect its potential as a therapeutic target for FM treatment.
Keywords: TRPV1; acupoint catgut embedding; fibromyalgia; medial prefrontal cortex (mPFC); phosphorylated endoplasmic reticulum kinase (pERK); somatosensory (SSC).