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电针抑制大鼠持续性炎症诱导的神经激肽-1受体的脊髓表达。

Electroacupuncture suppresses spinal expression of neurokinin-1 receptors induced by persistent inflammation in rats.

作者信息

Zhang Rui-Xin, Liu Bing, Qiao Jian-Tian, Wang Linbo, Ren Ke, Berman Brian M, Lao Lixing

机构信息

Center for Integrative Medicine, School of Medicine, University of Maryland, 3rd Floor, James Kernan Hospital, 2200 Kernan Drive, Baltimore, MD 21207, USA.

出版信息

Neurosci Lett. 2005 Aug 26;384(3):339-43. doi: 10.1016/j.neulet.2005.05.001.

Abstract

It has been demonstrated that electroacupuncture (EA) significantly suppresses behavioral hyperalgesia in a rat model of persistent inflammatory pain and that neurokinin-1 (NK-1)/substance P (SP) receptors play important roles in nociception and hyperalgesia at the spinal cord level. The present study investigated spinal NK-1 receptor involvement in EA-produced suppression of hyperalgesia in a rat model of persistent inflammatory pain. The results showed that hind paw inflammation induced a significant increase of NK-1 receptor expression in the spinal dorsal horn and that this effect was significantly suppressed by EA. This suggests that EA-induced suppression of hyperalgesia is involved, at least partly, in the suppression of the spinal NK-1 receptors induced by sustained peripheral nociceptive input.

摘要

业已证实,在持续性炎性疼痛大鼠模型中,电针(EA)可显著抑制行为性痛觉过敏,且神经激肽-1(NK-1)/P物质(SP)受体在脊髓水平的伤害感受和痛觉过敏中发挥重要作用。本研究调查了脊髓NK-1受体在持续性炎性疼痛大鼠模型中电针产生的痛觉过敏抑制作用中的参与情况。结果显示,后爪炎症诱导脊髓背角NK-1受体表达显著增加,且这种效应被电针显著抑制。这表明,电针诱导的痛觉过敏抑制作用至少部分涉及由持续外周伤害性输入诱导的脊髓NK-1受体的抑制。

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