Docagne Fabian, Mestre Leyre, Loría Frida, Hernangómez Miriam, Correa Fernando, Guaza Carmen
Grupo de Neuroinmunología, Instituto Ramón y Cajal, CSIC-Avda Dr Arce, 37, 28002 Madrid, Spain.
Expert Opin Ther Targets. 2008 Feb;12(2):185-95. doi: 10.1517/14728222.12.2.185.
Cannabinoids have been shown to exert beneficial actions in different animal models of multiple sclerosis (MS). However, the use of cannabinoids compounds in human therapy is greatly limited by their psychoactivity. Thus, new hopes in MS therapy have arisen from the evidence for a cannabinoid receptor, termed CB2, which is devoid of psychoactive effects in animal models.
This review discusses the different mechanisms by which CB2 activation could induce therapeutic actions in MS.
Particular focus is given to the potential effects on inflammation/autoimmunity, remyelination and neuroprotection.
This review discusses the importance of glial cells in sustaining these effects, as well as the putative secondary effects that would limit the use of CB2 agonists in the treatment of MS.
大麻素已在多种多发性硬化症（MS）动物模型中显示出有益作用。然而，大麻素化合物在人类治疗中的应用因具有精神活性而受到极大限制。因此，一种名为CB2的大麻素受体在动物模型中无精神活性的证据为MS治疗带来了新希望。
本综述讨论CB2激活可在MS中诱导治疗作用的不同机制。
特别关注其对炎症/自身免疫、髓鞘再生和神经保护的潜在影响。
本综述讨论了神经胶质细胞在维持这些作用中的重要性，以及可能限制CB2激动剂用于MS治疗的继发效应。
