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靶向CB2受体和内源性大麻素系统治疗疼痛。

Targeting CB2 receptors and the endocannabinoid system for the treatment of pain.

作者信息

Anand Praveen, Whiteside Garth, Fowler Christopher J, Hohmann Andrea G

机构信息

Imperial College London, UK.

出版信息

Brain Res Rev. 2009 Apr;60(1):255-66. doi: 10.1016/j.brainresrev.2008.12.003. Epub 2008 Dec 25.

Abstract

The endocannabinoid system consists of the cannabinoid (CB) receptors, CB(1) and CB(2), the endogenous ligands anandamide (AEA, arachidonoylethanolamide) and 2-arachidonoylglycerol (2-AG), and their synthetic and metabolic machinery. The use of cannabis has been described in classical and recent literature for the treatment of pain, but the potential for psychotropic effects as a result of the activation of central CB(1) receptors places a limitation upon its use. There are, however, a number of modern approaches being undertaken to circumvent this problem, and this review represents a concise summary of these approaches, with a particular emphasis upon CB(2) receptor agonists. Selective CB(2) agonists and peripherally restricted CB(1) or CB(1)/CB(2) dual agonists are being developed for the treatment of inflammatory and neuropathic pain, as they demonstrate efficacy in a range of pain models. CB(2) receptors were originally described as being restricted to cells of immune origin, but there is evidence for their expression in human primary sensory neurons, and increased levels of CB(2) receptors reported in human peripheral nerves have been seen after injury, particularly in painful neuromas. CB(2) receptor agonists produce antinociceptive effects in models of inflammatory and nociceptive pain, and in some cases these effects involve activation of the opioid system. In addition, CB receptor agonists enhance the effect of mu-opioid receptor agonists in a variety of models of analgesia, and combinations of cannabinoids and opioids may produce synergistic effects. Antinociceptive effects of compounds blocking the metabolism of anandamide have been reported, particularly in models of inflammatory pain. There is also evidence that such compounds increase the analgesic effect of non-steroidal anti-inflammatory drugs (NSAIDs), raising the possibility that a combination of suitable agents could, by reducing the NSAID dose needed, provide an efficacious treatment strategy, while minimizing the potential for NSAID-induced gastrointestinal and cardiovascular disturbances. Other potential "partners" for endocannabinoid modulatory agents include alpha(2)-adrenoceptor modulators, peroxisome proliferator-activated receptor alpha agonists and TRPV1 antagonists. An extension of the polypharmacological approach is to combine the desired pharmacological properties of the treatment within a single molecule. Hopefully, these approaches will yield novel analgesics that do not produce the psychotropic effects that limit the medicinal use of cannabis.

摘要

内源性大麻素系统由大麻素(CB)受体CB1和CB2、内源性配体花生四烯酸乙醇胺(AEA)和2-花生四烯酸甘油酯(2-AG)及其合成和代谢机制组成。大麻用于治疗疼痛在经典文献和近期文献中均有记载,但由于中枢CB1受体激活会产生精神效应,这限制了其应用。然而,目前正在采取多种现代方法来解决这一问题,本综述简要总结了这些方法,尤其着重介绍了CB2受体激动剂。选择性CB2激动剂以及外周选择性CB1或CB1/CB2双重激动剂正在研发用于治疗炎症性疼痛和神经性疼痛,因为它们在一系列疼痛模型中均显示出疗效。CB2受体最初被认为仅存在于免疫细胞中,但有证据表明其在人类初级感觉神经元中表达,并且在人类外周神经损伤后,尤其是在疼痛性神经瘤中,CB2受体水平会升高。CB2受体激动剂在炎症性疼痛和伤害性疼痛模型中产生抗伤害感受作用,在某些情况下,这些作用涉及阿片系统的激活。此外,CB受体激动剂在多种镇痛模型中增强了μ-阿片受体激动剂的作用,大麻素与阿片类药物联合使用可能产生协同效应。有报道称,阻断花生四烯酸乙醇胺代谢的化合物具有抗伤害感受作用,尤其是在炎症性疼痛模型中。还有证据表明,此类化合物可增强非甾体抗炎药(NSAIDs)的镇痛效果,这增加了一种可能性,即通过减少所需的NSAIDs剂量,合适药物的联合使用可提供一种有效的治疗策略,同时将NSAIDs引起的胃肠道和心血管紊乱的可能性降至最低。内源性大麻素调节剂的其他潜在“伙伴”包括α2-肾上腺素能受体调节剂、过氧化物酶体增殖物激活受体α激动剂和TRPV1拮抗剂。多药理学方法的一个拓展是将治疗所需的药理特性整合到单个分子中。有望这些方法能产生不会产生限制大麻药用的精神效应的新型镇痛药。

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