2020
DOI: 10.1155/2020/7061972
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Electroacupuncture Alleviates Experimental Chronic Inflammatory Pain by Inhibiting Calcium Voltage‐Gated Channel‐Mediated Inflammation

Abstract: Background. Both experimental and clinical studies have shown that electroacupuncture (EA) administration ameliorates chronic inflammatory pain (CIP). However, the multifaceted mechanism underlying the effects of EA on CIP is poorly understood. In this study, the mRNA transcriptome was used to study various therapeutic targets of EA. Methods. Using RNA-sequencing, protein-coding mRNA expression profiles of the L4-L5 dorsal root ganglion (DRG) were examined in the control (CN), complete Freund’s adjuvant- (CFA-… Show more

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Cited by 8 publications
(5 citation statements)
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“…In this study, GSEA results showed that CHRNA3 was enriched in neuroactive ligand-receptor interaction, ECM-receptor interaction, and IL-17 signaling pathway-related pathways, while CHRNB2 and CHRNB4 were related to ferroptosis, the toll-like receptor signaling pathway, the hedgehog signaling pathway, cell cycle, the mTOR signaling pathway, and inflammatory mediator regulation of TRP channels, respectively. Most of these signaling pathways mediate nerve injury and the continuation of NPP by participating in neurotoxicity [ 31 ], neural activity [ 32 ], inflammatory response [ 33 , 34 ], hyperalgesia [ 35 ], nerve healing [ 36 , 37 ], microglia polarization [ 38 ], and oxidative stress [ 39 ].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In this study, GSEA results showed that CHRNA3 was enriched in neuroactive ligand-receptor interaction, ECM-receptor interaction, and IL-17 signaling pathway-related pathways, while CHRNB2 and CHRNB4 were related to ferroptosis, the toll-like receptor signaling pathway, the hedgehog signaling pathway, cell cycle, the mTOR signaling pathway, and inflammatory mediator regulation of TRP channels, respectively. Most of these signaling pathways mediate nerve injury and the continuation of NPP by participating in neurotoxicity [ 31 ], neural activity [ 32 ], inflammatory response [ 33 , 34 ], hyperalgesia [ 35 ], nerve healing [ 36 , 37 ], microglia polarization [ 38 ], and oxidative stress [ 39 ].…”
Section: Discussionmentioning
confidence: 99%
“…In this study, GSEA results showed that CHRNA3 was enriched in neuroactive ligandreceptor interaction, ECM-receptor interaction, and IL-17 signaling pathway-related pathways, while CHRNB2 and CHRNB4 were related to ferroptosis, the toll-like receptor signaling pathway, the hedgehog signaling pathway, cell cycle, the mTOR signaling pathway, and inflammatory mediator regulation of TRP channels, respectively. Most of these signaling pathways mediate nerve injury and the continuation of NPP by participating in neurotoxicity [31], neural activity [32], inflammatory response [33,34], hyperalgesia [35], nerve healing [36,37], microglia polarization [38], and oxidative stress [39]. e nicotine and nicotinic acetylcholine receptors (NAChRs) subtype, by a variety of subunits of combinatorial synthesis channel receptor complexes, its structure, and function in the nervous system of diversity, had been found to enhance the presynaptic neurotransmitter and release and affect the excitability of neurons, and when its function declines, it would cause the nervous system dysfunction [40,41].…”
Section: Discussionmentioning
confidence: 99%
“…Notably, myalgias, headache and abdominal pain are all symptoms of COVID-19 [ 16 ], which can be regulated by calcium signaling pathway and neuroactive ligand–receptor interaction [ 17 ]. A study using RNA-sequencing found that experimental chronic inflammatory pain could be relieved by electroacupuncture via the suppression of calcium voltage-gated channel-mediated inflammation [ 90 ]. Although most calcium signaling pathway studies focused on pain and cardiovascular disease research, it has also been shown to be associated with inflammatory responses [ 29 ].…”
Section: Discussionmentioning
confidence: 99%
“…Glutamatergic synaptic transmission is coupled with excess Ca 2+ entry into projection neurons and results in the activation of the Ca 2+ -dependent enzyme Ca 2+ /calmodulin-dependent protein kinase II (CamKII) and phosphorylation of the NR2B subunit of NMDAR at postsynaptic sites in the ACC, thus modulating visceral pain in a viscerally hypersensitive model [ 80 ]. It was reported that EA at ST36 and Kunlun (BL60) could reverse the actions of the calcium voltage-gated channel subunit and calcium voltage-gated channel auxiliary subunit γ , thus reducing chronic inflammatory pain (CIP) in the CFA rats [ 47 ].…”
Section: Central Sensitization In Pain Transmission and Modulationmentioning
confidence: 99%