Abstract
Although inflammatory pain is a common clinical condition, its mechanisms are still unclear. Electroacupuncture (EA), a well-known method of pain management, may reduce inflammatory pain by regulating neurons, astrocytes, and inflammatory signaling pathways. Injections of complete Freund’s adjuvant (CFA), which can initiate cell-mediated inflammatory pain, resulted in significant hyperalgesia, which was subsequently prevented by EA. In CFA-injected mice, a dramatic increase was observed in the expression of the following proteins in the dorsal root ganglion and spinal cord dorsal horn: the astrocytic marker GFAP, S100B, RAGE, pPKCε, COX-2, pERK, and pNFκB. These effects were reversed by EA. In addition, mechanical hyperalgesia was significantly reduced in the N6-cyclopentyladenosine (CPA) i.p. or i.m. and endomorphin (EM) i.p. groups. Neither EM i.m. nor EM i.p. exhibited any analgesic effect on thermal hyperalgesia. However, both CPA i.m. and CPA i.p. attenuated thermal hyperalgesia in the mouse inflammatory pain model. We showed that CPA reduced COX-2 and pPKCε expression. However, EM administration did not reduce COX-2 levels. Combined administration of naloxone and rolofylline increased pPKCε and COX-2 pathways. Taken together, our study results revealed a novel and detailed mechanism of EA-induced analgesia that involves the regulation of the opioid and adenosine pathways.
Highlights
Mechanisms for spinal inflammatory factors, endogenous opioids, and adenosine remain unclear
One study has revealed that the prostaglandin E2 binds to G-proteins, resulting in a subsequent increase in cyclic AMP levels and consequent activation of PKC signaling pathways and purinergic 2X3 (P2X3) receptors; this causes exaggerated hyperalgesia[17]
The present study aimed to identify the role of EA on inflammatory pain in mice and the effects of EA on the regulation of neurons, astrocytes, and other inflammatory signaling pathways
Summary
Mechanisms for spinal inflammatory factors, endogenous opioids, and adenosine remain unclear. A previous study has indicated that following tissue injury or infection, immune cells secrete inflammatory mediators, such as proinflammatory cytokines, bradykinin, and prostaglandins These inflammatory mediators act on their respective receptors on peripheral nociceptor neural fibers. Researchers have found that enkephalin activates the presynaptic δ-opioid receptor and inhibits nociceptive VGSC 1.7 in the dorsal root ganglion (DRG) through PKC and p38 inhibition[14] Both PKA and PKC are involved in the modulation of Nav1.8 currents from neonatal neurons[15,16]. COX-2 is an inflammation-related enzyme that transforms arachidonic acid into different types of prostaglandins, including I2 and E2 These proinflammatory mediators cause inflammation and pain. It is clinically acknowledged that non-steroidal anti-inflammatory drugs can relieve dysmenorrhea and migraines It is unknown whether early use of acupuncture can prevent pain generation in such conditions. The present study aimed to identify the role of EA on inflammatory pain in mice and the effects of EA on the regulation of neurons, astrocytes, and other inflammatory signaling pathways
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