Abstract
Fibromyalgia is characterized by chronic and persistent widespread pain and generalized muscle tenderness, and it is refractory to treatment. The central nervous system (CNS) plays an important role, pain signalling, in fibromyalgia subjects. Electroacupuncture (EA) has been practiced for thousand years to treat many diseases that involve pain. We established fibromyalgia-like pain in mice using intermittent cold stress and investigated therapeutic effects and modes of action with EA. EA of 2 Hz and 1 mA was performed for 20 min at the ST36 acupoint in mice from Day 3 to Day 5. Our results showed that mechanical and thermal hyperalgesia were induced by intermittent cold stress (Day 5: mechanical: 1.43 ± 0.34 g; thermal: 3.98 ± 0.73 s) and were subsequently reversed by EA (Day 5: mechanical: 4.62 ± 0.48 g; thermal: 7.68 ± 0.68 s) or Trpv1−/− (Day 5: mechanical: 4.38 ± 0.51 g; thermal: 7.48 ± 0.98 s). Activity in the HMGB1, S100B, and TRPV1 pathways was increased in the mouse prefrontal cortex, somatosensory cortex, thalamus, and amygdala with the stress treatment. This increase was attenuated by EA or Trpv1−/−. These results suggest potential targets for the treatment of TRPV1-dependant fibromyalgia pain.
Highlights
Fibromyalgia, called fibromyalgia syndrome, is characterized by chronic widespread pain, severe fatigue, and sleep disturbances
After the final behavior test, remainder euthanized with a 5% isoflurane via inhalation and intracardially perfused with normal saline followed by 4% paraformaldehyde. e brain was immediately dissected and postfixed with 4% paraformaldehyde at 4°C for 3 days. e tissues were placed in 30% sucrose for cryoprotection overnight at 4°C. e brain was embedded in an optimal cutting temperature (OCT) compound and rapidly frozen using liquid nitrogen before storing the tissues at −80°C
We showed that CSP increased Toll-like receptor 2 (TLR2) and pNF-κB. Activated NF-κB (pNF-κB) expression (Figure 2(b)). is overexpression was reduced by EA and Trpv1−/− (Figure 2(b), #P < 0.05, n 3)
Summary
Fibromyalgia, called fibromyalgia syndrome, is characterized by chronic widespread pain, severe fatigue, and sleep disturbances. HMGB1 is considered to be a cytokine released from necrotic cells or secreted by immunocompetent cells activated by interleukin-1 (IL-1), interferon-c (IFN-c), tumor necrosis factor α (TNF-α), or endotoxin [12] It targets cell surface receptors, such as receptor for advanced glycation end-products (RAGE), Toll-like receptor 2 (TLR2), and TLR4, to activate cytoplasmic signalling cascades that result in the modulation of DNA transcription by nuclear factor-κB (NF-κB). Cold stress augmented inflammatory modulators, such as HMGB1 and S100B, contribute to the pain process by activating TLR4 and RAGE. E current study aimed to examine the effect of EA on cold stress-induced fibromyalgia pain in mice. E present study aimed to investigate whether EA reduces fibromyalgia pain by inhibiting the HMGB1, S100B, and TRPV1 signalling pathways in the mouse brain. Our results provided evidence that TRPV1 might be a potential target for developing effective pain treatments
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