Pryce Gareth, Ahmed Zubair, Hankey Deborah J R, Jackson Samuel J, Croxford J Ludovic, Pocock Jennifer M, Ledent Catherine, Petzold Axel, Thompson Alan J, Giovannoni Gavin, Cuzner M Louise, Baker David
Department of Neuroinflammation, Institute of Neurology, University College London, London, UK.
Brain. 2003 Oct;126(Pt 10):2191-202. doi: 10.1093/brain/awg224. Epub 2003 Jul 22.
Multiple sclerosis is increasingly being recognized as a neurodegenerative disease that is triggered by inflammatory attack of the CNS. As yet there is no satisfactory treatment. Using experimental allergic encephalo myelitis (EAE), an animal model of multiple sclerosis, we demonstrate that the cannabinoid system is neuroprotective during EAE. Mice deficient in the cannabinoid receptor CB1 tolerate inflammatory and excitotoxic insults poorly and develop substantial neurodegeneration following immune attack in EAE. In addition, exogenous CB1 agonists can provide significant neuroprotection from the consequences of inflammatory CNS disease in an experimental allergic uveitis model. Therefore, in addition to symptom management, cannabis may also slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis and probably other diseases.
多发性硬化症越来越被认为是一种由中枢神经系统炎症攻击引发的神经退行性疾病。目前尚无令人满意的治疗方法。利用实验性自身免疫性脑脊髓炎（EAE），一种多发性硬化症的动物模型，我们证明大麻素系统在EAE期间具有神经保护作用。缺乏大麻素受体CB1的小鼠对炎症和兴奋性毒性损伤的耐受性较差，在EAE的免疫攻击后会发生大量神经退行性变。此外，外源性CB1激动剂可以在实验性过敏性葡萄膜炎模型中为炎症性中枢神经系统疾病的后果提供显著的神经保护。因此，除了症状管理外，大麻还可能减缓最终导致多发性硬化症以及可能其他疾病慢性残疾的神经退行性过程。
