Ito S, Okuda-Ashitaka E, Minami T
Department of Medical Chemistry, Kansai Medical University, 10-15 Fumizono, Moriguchi 570-8506, Japan.
Neurosci Res. 2001 Dec;41(4):299-332. doi: 10.1016/s0168-0102(01)00289-9.
While acute pain has a fundamental role to operate a protective system, chronic pain associated with inflammation and nerve injury often outlasts its biological usefulness. Therefore, there has recently been great interest in the neurochemical mechanisms of hyperalgesia to noxious stimuli and tactile pain (allodynia) to innocuous stimuli with a hope to relieve persistent, intractable pain. Over several decades non-steroidal anti-inflammatory drugs and opioids have been employed for clinical management of pain. The introduction of molecular biology to pain research has enabled us to describe the mechanism of pain at the molecular level and to develop analgesics with selectivity for targets and with less adverse effects. This review focuses on current knowledge concerning mechanisms and pathways for pain induced by prostaglandins and their interactions with novel neuropeptides nociceptin/orphanin FQ and nocistatin derived from the same opioid precursor protein.
虽然急性疼痛在启动保护系统方面具有重要作用,但与炎症和神经损伤相关的慢性疼痛往往会持续超出其生物学效用的时间。因此,最近人们对有害刺激引起的痛觉过敏以及无害刺激引起的触觉疼痛(异常性疼痛)的神经化学机制产生了浓厚兴趣,以期缓解持续性、顽固性疼痛。几十年来,非甾体类抗炎药和阿片类药物一直被用于疼痛的临床管理。分子生物学引入疼痛研究,使我们能够在分子水平上描述疼痛机制,并开发出对靶点具有选择性且副作用较小的镇痛药。本综述聚焦于当前有关前列腺素诱导疼痛的机制和途径,以及它们与源自同一阿片样前体蛋白的新型神经肽痛敏肽/孤啡肽FQ和痛抑素相互作用的相关知识。