Abstract
BackgroundThe treatment, and efficacy thereof, is considered to be inadequate with specificity to alleviation of Fibromyalgia and its associated pain. Fibromyalgia patients suffer from chronic and persistent widespread pain and generalized tenderness. Transient receptor potential V1 (TRPV1), which is reported as a Ca2+ permeable ion channel that can be activated by inflammation, is reported to be involved in the development of fibromyalgia pain.MethodsThe current study explored the TRPV1 channel functions as a noxious sensory input in mice cold stress model. It remains unknown whether electroacupuncture (EA) attenuates fibromyalgia pain or affects the TRPV1 pathway.ResultsWe show that cold stress increases mechanical and thermal pain (day 7: mechanical: 1.69 ± 0.41 g; thermal: 4.68 ± 0.56 s), and that EA and Trpv1 deletion counter this increase. EA and Trpv1 deletion reduced the cold stress-induced increase in inflammatory mediators and TRPV1-related molecules in the hypothalamus, periaqueductal gray (PAG), and cerebellum of mice.ConclusionsOur results imply that EA has an analgesic effect associated with TRPV1 downregulation. We provide novel evidence that these inflammatory mediators can modulate the TRPV1 signaling pathway and suggest new potential therapeutic targets for fibromyalgia pain.
Highlights
Fibromyalgia pain lacks objective parameters for diagnosis and therapeutic effect evaluation
The von Frey test revealed that EA and Trpv1 deletion substantially attenuated the typical intermediate cold stress-induced mechanical hyperalgesia (Fig. 1A, D7: EA group: 4.76 ± 0.28, Trpv1−/− group: 4.49 ± 0.51, n = 10)
We examined whether EA or Trpv1 deletion altered thermal hyperalgesia in cold stress pain (CSP) mice
Summary
Fibromyalgia pain lacks objective parameters for diagnosis and therapeutic effect evaluation. Its major symptoms are persistent widespread mechanical and thermal hyperalgesia and generalized tenderness. The high mobility group box-1 (HMGB1) is a crucial inflammatory mediator in several pain conditions and often presents with an enhanced immune. S100B (a protein released by microglia) has been established to be involved in the inflammatory process within the CNS of rats [10]. S100B can activate the receptor for advanced glycation end-products (RAGE), which increase the Interleukin-1β (IL-1β) and Tumor Necrosis Factor-α (TNF-α) levels, activating the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NFkB) in microglia [12]. Fibromyalgia patients suffer from chronic and persistent widespread pain and generalized tenderness. Transient receptor potential V1 (TRPV1), which is reported as a C a2+ permeable ion channel that can be activated by inflammation, is reported to be involved in the development of fibromyalgia pain
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