Objectives
Chronic pain has a definitive lack of objective parameters in the measurement and treatment efficacy of diseases such as inflammatory and fibromyalgia (FM) pain. This disease has indicated a refractory tendency to conventional treatment ventures, largely resultant from a lack of etiological and pathogenic understanding of the disease development. Emerging evidence indicates that the central nervous system (CNS) plays a critical role in the amplification of pain signals. It remains unclear whether or not electroacupuncture (EA) can attenuate the chronic pain associated with inflammatory and FM pain.
Methods
We examined the contribution of the transient receptor potential vanalloid 1 (TRPV1) channel to inflammatory and fibromyalgia-like pain in inflammatory and intermittent cold-stress (ICS) model, in the prefrontal cortex, somatosensory cortex, hippocampus and thalamus areas of the brain. The potential therapeutic benefits of electroacupuncture (EA) was analysed in order to identify the analgesic effects and mechanism.
Results
We suggest that TRPV1 upregulation is central to the inflammatory and FM pain induced hyperalgesia and the treatment of EA showed a decrease in these pain induced nociceptive sensitization, suggesting TRPV1 and related nociceptive conduit upregulation and overexpression can be attenuated by EA. The results indicate that EA treatment successfully attenuated both mechanical and thermal hyperalgesia. A majority of proteins associated with the nociceptive signalling cascade indicated overexpression in inflammatory and FM pain, which was rescued through the use of EA. The use of TRPV1 knockout mice allowed for a successful blockade of TRPV1 expression, and further served to elucidate the role of the TRPV1 receptor in the development and expression of inflammatory and FM-like pain. This evidence strongly suggests that the TRPV1 signalling pathway and related components may represent promising therapeutic targets for FM treatment.
Conclusion
Furthermore, the treatment of EA showed a decrease in the inflammatory and FM induced nociceptive sensitization, suggesting TRPV1 upregulation and overexpression can be attenuated by EA at bilateral ST36, and that EA can provide analgesic benefits to patients suffering from inflammatory and FM pain.