School of Biomedical Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK.
PPAR Res. 2007;2007:23513. doi: 10.1155/2007/23513.
Cannabinoids have been used medicinally and recreationally for thousands of years and their effects were proposed to occur mainly via activation of the G-protein-coupled receptor CB1/CB2 (cannabinoid receptor 1/2). Discovery of potent synthetic analogs of the natural cannabinoids as clinically useful drugs is the sustained aim of cannabinoid research. This demands that these new compounds be free of the psychotropic effects that connected with the recreational use of cannabinoids. In preclinical studies cannabinoids displayed many of the characteristics of nonsteroidal anti-inflammatory drugs (NSAIDs) and it seems to be free of unwanted side effects. An increasing number of therapeutic actions of cannabinoid are being reported that do not appear to be mediated by either CB1 or CB2, and recently nuclear receptor superfamily PPARs (peroxisome-proliferator-activated receptors) have been suggested as the target of certain cannabinoids. This review summarizes the evidence for cannabinoid activation on PPARs and possible associated remedial potentials.
大麻素在医学和娱乐方面已经使用了数千年,其作用主要通过激活 G 蛋白偶联受体 CB1/CB2(大麻素受体 1/2)来实现。发现具有天然大麻素临床应用潜力的有效合成类似物是大麻素研究的持续目标。这要求这些新化合物没有与大麻素娱乐性使用相关的精神作用。在临床前研究中,大麻素显示出许多非甾体抗炎药(NSAIDs)的特征,而且似乎没有不必要的副作用。越来越多的大麻素治疗作用被报道,这些作用似乎不是由 CB1 或 CB2 介导的,最近核受体超家族 PPARs(过氧化物酶体增殖物激活受体)被认为是某些大麻素的靶点。这篇综述总结了大麻素对 PPARs 的激活作用及其可能的相关治疗潜力的证据。