首页> 外文期刊>Brain research >Involvement of nociceptin/orphanin FQ and its receptor in electroacupuncture-produced anti-hyperalgesia in rats with peripheral inflammation.
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Involvement of nociceptin/orphanin FQ and its receptor in electroacupuncture-produced anti-hyperalgesia in rats with peripheral inflammation.

机译:Nociceptin / orphanin FQ及其受体与周围炎症大鼠电针产生的抗痛觉过敏有关。

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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.
机译:N / OFQ肽受体(NOP受体)的内源性激动剂神经肽伤害感受素/孤儿蛋白FQ(N / OFQ)已被证明参与许多生理和病理功能,包括疼痛调节。在本研究中,在患有周围炎症的大鼠中研究了N / OFQ-NOP受体系统在电针(EA)产生的抗痛觉过敏中的作用。鞘内(it)在GB30和GB34穴位处施用N / OFQ(15 nmol)或EA可以显着减轻痛觉过敏,这是通过向一只大鼠的皮下注射完全弗氏佐剂(CFA)诱导的,表现为爪缩回潜伏期(PWL)降低)对有害的热刺激。鞘内注射NOP受体的选择性拮抗剂[Nphe(1)] nociceptin(1-13)NH(2)(20 nmol)可显着阻断N / OFQ或EA的抗伤害作用。受体介导的机制。此外,与单独使用每种成分产生的痛觉过敏相比,N / OFQ注射与EA治疗相结合可以增强抗痛觉过敏。这些发现表明,脊髓N / OFQ-NOP系统可能参与了EA镇痛,这可能是EA抑制大鼠外周炎症性疼痛的机制之一。

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