Abstract
Transient receptor potential vanilloid 1 (TRPV1) and associated signaling pathways have been reported to be increased in inflammatory pain signaling. There are accumulating evidences surrounding the therapeutic effect of electroacupuncture (EA). EA can reliably attenuate the increase of TRPV1 in mouse inflammatory pain models with unclear signaling mechanisms. Moreover, the difference in the clinical therapeutic effects between using the contralateral and ipsilateral acupoints has been rarely studied. We found that inflammatory pain, which was induced by injecting the complete Freund’s adjuvant (CFA), (2.14 ± 0.1, p < 0.05, n = 8) can be alleviated after EA treatment at either ipsilateral (3.91 ± 0.21, p < 0.05, n = 8) or contralateral acupoints (3.79 ± 0.25, p < 0.05, n = 8). EA may also reduce nociceptive Nav sodium currents in dorsal root ganglion (DRG) neurons. The expression of TRPV1 and associated signaling pathways notably increased after the CFA injection; this expression can be further attenuated significantly in EA treatment. TRPV1 and associated signaling pathways can be prevented in TRPV1 knockout mice, suggesting that TRPV1 knockout mice are resistant to inflammatory pain. Through this study, we have increased the understanding of the mechanism that both ipsilateral and contralateral EA might alter TRPV1 and associated signaling pathways to reduce inflammatory pain.
Highlights
Transient receptor potential vanilloid 1 (TRPV1) is a ion channel that is expressed in nociceptive neurons in the dorsal root ganglion (DRG), dorsal horn of the spinal cord (SCDH), the brain, and peripheral tissue[3,13]
We found that EA can reduce inflammatory pain induced by complete Freund’s adjuvant (CFA) and alleviate nociceptive Nav sodium currents
Mechanical and thermal hyperalgesia induced by CFA injection was suppressed by both ipsilateral and contralateral EA treatments
Summary
TRPV1 is a ion channel that is expressed in nociceptive neurons in the dorsal root ganglion (DRG), dorsal horn of the spinal cord (SCDH), the brain, and peripheral tissue[3,13]. Recent study found that thermal and mechanical hyperalgesia caused by CFA-induced inflammation led to increased TRPV1 expression in DRG neurons for 28 days[19]. Yang et al studied contralateral acupuncture in 2011, and they found that low frequency EA could reduce hyperalgesia induced by carrageenan and that the mechanism for the pain reduction used μ-opioid receptors in the SC30. Due to its effectiveness in analgesia, people have investigated the mechanisms of pain relief acupuncture. Theories have been proposed and studies have been conducted about contralateral acupuncture, they did not mention the difference between using ipsilateral and contralateral acupoints. The purpose of this study was to investigate whether there was a difference in analgesic effect following acupuncture at an ipsilateral acupoint compared to a contralateral acupoint. Aforementioned mechanisms might be crucial and clear methods pertaining to EA analgesia
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