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首页> 外文期刊>Scientific reports. >Probing the Effects and Mechanisms of Electroacupuncture at Ipsilateral or Contralateral ST36–ST37 Acupoints on CFA-induced Inflammatory Pain
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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IpsilateLeral或对侧ST36-ST37穴位对CFA诱导的炎症疼痛的影响和机制

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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:据报道,瞬时受体潜在的香草素1(TRPV1)和相关的信号传导途径在炎性疼痛信号中增加。覆盖电针(EA)的治疗效果周围存在积累证据。 EA可以可靠地衰减小鼠炎症疼痛模型的TRPV1增加,信号传导机制。此外,使用对侧和同侧穴位之间的临床治疗效果的差异很少已经研究过。我们发现通过注射完整的弗氏佐剂(CFA)诱导的炎症疼痛(2.14±0.1,P <0.05,n = 8),可以在EA治疗后进行缓解(3.91±0.21,p <0.05, n = 8)或对侧穴位(3.79±0.25,p <0.05,n = 8)。 EA也可能减少背根神经节(DRG)神经元中的伤害性导航钠电流。在CFA注射后,TRPV1和相关信号传导途径的表达显着增加;在EA治疗中可以显着衰减该表达。在TRPV1敲除小鼠中可以防止TRPV1和相关的信号传导途径,表明TRPV1敲除小鼠对炎症疼痛抵抗力。通过这项研究,我们提高了对同侧和对侧EA可以改变TRPV1和相关的信号通路来降低炎症疼痛的机制的理解。

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