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Probing the Effects and Mechanisms of Electroacupuncture at Ipsilateral or Contralateral ST36–ST37 Acupoints on CFA-induced Inflammatory Pain

机译:探讨同侧或对侧ST36-ST37穴位电针治疗CFA引起的炎性疼痛的作用及其机制

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摘要

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.
机译:瞬态受体电位香草酸1(TRPV1)和相关的信号通路已被报告增加炎症性疼痛信号。围绕电针(EA)的治疗作用有越来越多的证据。 EA可以可靠地减弱小鼠炎症性疼痛模型中TRPV1的表达,信号机制尚不清楚。此外,很少研究使用对侧和同侧穴位之间的临床治疗效果差异。我们发现,在任何同侧(3.91±0.21,p <0.05,)EA治疗后,通过注射完全弗氏佐剂(CFA)(2.14±0.1,p <0.05,n = 8)引起的炎症性疼痛可以缓解。 n = 8)或对侧穴位(3.79±0.25,p <0.05,n = 8)。 EA还可以减少背根神经节(DRG)神经元的伤害性Nav钠电流。注射CFA后TRPV1的表达和相关信号通路明显增加;该表达在EA治疗中可进一步显着减弱。 TRPV1基因敲除小鼠中可以防止TRPV1和相关的信号通路,这表明TRPV1基因敲除小鼠对炎性疼痛具有抵抗力。通过这项研究,我们加深了对同侧和对侧EA可能改变TRPV1和相关信号传导途径以减轻炎症性疼痛的机制的了解。

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