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孤啡肽及其受体在电针对外周炎症大鼠产生的抗痛觉过敏中的作用

Involvement of nociceptin/orphanin FQ and its receptor in electroacupuncture-produced anti-hyperalgesia in rats with peripheral inflammation.

作者信息

Fu Xin, Wang Yan-Qing, Wu Gen-Cheng

机构信息

Department of Integrative Medicine and Neurobiology, Institute of Acupuncture Research, Shanghai Medical College, Fudan University, P.O. Box 291, 138, Yi Xue Yuan Road, Shanghai 200032, China.

出版信息

Brain Res. 2006 Mar 17;1078(1):212-8. doi: 10.1016/j.brainres.2006.01.026. Epub 2006 Mar 24.

Abstract

The neuropeptide nociceptin/orphanin FQ (N/OFQ), the endogenous agonist of the N/OFQ peptide receptor (NOP receptor), has been demonstrated to be involved in many physiological and pathological functions including pain regulation. In the present study, the involvement of N/OFQ-NOP receptor system in electroacupuncture (EA)-produced anti-hyperalgesia was investigated in rats with peripheral inflammation. Intrathecal (i.t.) administration of N/OFQ (15 nmol) or EA at acupoints GB30 and GB34 could significantly attenuate hyperalgesia which was induced by subcutaneously injecting complete Freund's adjuvant (CFA) into one hindpaw of rats, manifesting as decreased paw withdrawal latency (PWL) to the noxious thermal stimulus. The anti-nociceptive effect of N/OFQ or EA was significantly blocked by intrathecal injection of [Nphe(1)]nociceptin(1-13)NH(2) (20 nmol), a selective antagonist of the NOP receptor, indicating the NOP-receptor-mediated mechanism. Additionally, the combination of N/OFQ injection with EA treatment could enhance anti-hyperalgesia compared to that produced by each component alone. These findings suggested that the spinal N/OFQ-NOP system might be involved in EA analgesia, which may be one of the mechanisms underlying the anti-nociceptive effect of EA in rat's peripheral inflammatory pain.

摘要

神经肽痛敏肽/孤啡肽FQ(N/OFQ)是N/OFQ肽受体(NOP受体)的内源性激动剂,已被证明参与包括疼痛调节在内的多种生理和病理功能。在本研究中,研究了N/OFQ-NOP受体系统在电针(EA)诱导的外周炎症大鼠抗痛觉过敏中的作用。鞘内注射N/OFQ(15 nmol)或针刺足少阳胆经的环跳穴(GB30)和阳陵泉穴(GB34)可显著减轻皮下注射完全弗氏佐剂(CFA)至大鼠一侧后爪所诱导的痛觉过敏,表现为对有害热刺激的缩爪潜伏期(PWL)缩短。鞘内注射NOP受体选择性拮抗剂[苯丙氨酸(1)]痛敏肽(1-13)NH₂(20 nmol)可显著阻断N/OFQ或EA的抗伤害性感受作用,表明其通过NOP受体介导。此外,与单独使用每种成分相比,N/OFQ注射与EA治疗联合应用可增强抗痛觉过敏作用。这些结果提示,脊髓N/OFQ-NOP系统可能参与EA镇痛,这可能是EA对大鼠外周炎性疼痛产生抗伤害性感受作用的机制之一。

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