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通过激活过氧化物酶体增殖物激活受体α实现快速广谱镇痛

Rapid broad-spectrum analgesia through activation of peroxisome proliferator-activated receptor-alpha.

作者信息

LoVerme Jesse, Russo Roberto, La Rana Giovanna, Fu Jin, Farthing Jesse, Mattace-Raso Giuseppina, Meli Rosaria, Hohmann Andrea, Calignano Antonio, Piomelli Daniele

机构信息

Department of Pharmacology, Center for Drug Discovery, University of California, Irvine, CA 92697-4625, USA.

出版信息

J Pharmacol Exp Ther. 2006 Dec;319(3):1051-61. doi: 10.1124/jpet.106.111385. Epub 2006 Sep 22.

Abstract

Severe pain remains a major area of unmet medical need. Here we report that agonists of the nuclear receptor PPAR-alpha (peroxisome proliferator-activated receptor-alpha) suppress pain behaviors induced in mice by chemical tissue injury, nerve damage, or inflammation. The PPAR-alpha agonists GW7647 [2-(4-(2-(1-cyclohexanebutyl)-3-cyclohexylureido)ethyl)phenylthio)-2-methylpropionic acid], Wy-14643 [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthioacetic acid], and palmitoylethanolamide (PEA) reduced nocifensive behaviors elicited in mice by intraplantar (i.pl.) injection of formalin or i.p. injection of magnesium sulfate. These effects were absent in PPAR-alpha-null mice yet occurred within minutes of agonist administration in wild-type mice, suggesting that they were mediated through a transcription-independent mechanism. Consistent with this hypothesis, blockade of calcium-operated IK(ca) (K(Ca)3.1) and BK(ca) (K(Ca)1.1) potassium channels prevented the effects of GW7647 and PEA in the formalin test. Three observations suggest that PPAR-alpha agonists may inhibit nocifensive responses by acting on peripheral PPAR-alpha. (i) PEA reduced formalin-induced pain at i.pl. doses that produced no increase in systemic PEA levels; (ii) PPAR-alpha was expressed in dorsal root ganglia neurons of wild-type but not PPAR-alpha-null mice; and (ii) GW7647 and PEA prevented formalin-induced firing of spinal cord nociceptive neurons in rats. In addition to modulating nociception, GW7647 and PEA reduced hyperalgesic responses in the chronic constriction injury model of neuropathic pain; these effects were also contingent on PPAR-alpha expression and were observed following either acute or subchronic PPAR-alpha agonist administration. Finally, acute administration of GW7647 and PEA reduced hyperalgesic responses in the complete Freund's adjuvant and carrageenan models of inflammatory pain. Our results suggest that PPAR-alpha agonists may represent a novel class of analgesics.

摘要

剧痛仍然是医学上尚未满足的主要需求领域。在此我们报告,核受体PPAR-α(过氧化物酶体增殖物激活受体-α)激动剂可抑制化学组织损伤、神经损伤或炎症在小鼠中诱导的疼痛行为。PPAR-α激动剂GW7647 [2-(4-(2-(1-环己基丁基)-3-环己基脲基)乙基)苯硫基)-2-甲基丙酸]、Wy-14643 [4-氯-6-(2,3-二甲基苯胺基)-2-嘧啶基硫代乙酸]和棕榈酰乙醇胺(PEA)可减少小鼠因足底注射福尔马林或腹腔注射硫酸镁引起的伤害性防御行为。这些效应在PPAR-α基因敲除小鼠中不存在,但在野生型小鼠中给予激动剂后几分钟内就会出现,这表明它们是通过不依赖转录的机制介导的。与该假设一致,钙激活的IK(ca)(K(Ca)3.1)和BK(ca)(K(Ca)1.1)钾通道的阻断可阻止GW7647和PEA在福尔马林试验中的作用。三项观察结果表明,PPAR-α激动剂可能通过作用于外周PPAR-α来抑制伤害性防御反应。(i)PEA在足底注射剂量下可减轻福尔马林诱导的疼痛,而全身PEA水平并未升高;(ii)PPAR-α在野生型小鼠的背根神经节神经元中表达,但在PPAR-α基因敲除小鼠中不表达;(iii)GW7647和PEA可阻止福尔马林诱导的大鼠脊髓伤害性神经元放电。除了调节痛觉外,GW7647和PEA还可减轻神经性疼痛慢性压迫损伤模型中的痛觉过敏反应;这些效应也取决于PPAR-α的表达,并且在急性或亚慢性给予PPAR-α激动剂后均可观察到。最后,急性给予GW7647和PEA可减轻完全弗氏佐剂和角叉菜胶炎症性疼痛模型中的痛觉过敏反应。我们的结果表明,PPAR-α激动剂可能代表一类新型镇痛药。

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