O'Sullivan Saoirse Elizabeth
School of Medicine, Royal Derby Hospital, University of Nottingham.
Br J Pharmacol. 2016 Jun;173(12):1899-910. doi: 10.1111/bph.13497. Epub 2016 May 19.
Some cannabinoids activate the different isoforms of PPARs (α, β and γ), as shown through the use of reporter gene assays, binding studies, selective antagonists and knockout studies. Activation of all isoforms, but primarily PPARα and γ, mediates some (but not all) of the analgesic, neuroprotective, neuronal function modulation, anti-inflammatory, metabolic, anti-tumour, gastrointestinal and cardiovascular effects of some cannabinoids, often in conjunction with activation of the more traditional target sites of action such as the cannabinoid CB1 and CB2 receptors and the TRPV1 ion channel. PPARs also mediate some of the effects of inhibitors of endocannabinoid degradation or transport. Cannabinoids may be chaperoned to the PPARs by fatty acid binding proteins. The aims of this review are to update the evidence supporting PPAR activation by cannabinoids and to review the physiological responses to cannabinoids that are mediated, and not mediated, by PPAR activation.
一些大麻素可激活过氧化物酶体增殖物激活受体（PPARs）的不同亚型（α、β和γ），这已通过报告基因检测、结合研究、选择性拮抗剂和基因敲除研究得到证实。所有亚型的激活，尤其是PPARα和γ的激活，介导了一些（但并非全部）大麻素的镇痛、神经保护、神经元功能调节、抗炎、代谢、抗肿瘤、胃肠道和心血管作用，这些作用通常与激活更传统的作用靶点（如大麻素CB1和CB2受体以及TRPV1离子通道）同时发生。PPARs还介导了内源性大麻素降解或转运抑制剂的一些作用。脂肪酸结合蛋白可能会将大麻素转运至PPARs。本综述的目的是更新支持大麻素激活PPARs的证据，并综述由PPAR激活介导和未介导的大麻素生理反应。
