科学家最新研究发现，大麻中的化学物质能用于治疗人类多发性硬化症（MS），这一发现能大大提高治疗的效果，因为大麻物质不但能减少神经损伤以及异常神经冲动产生，更重要的是它能阻止疾病的进一步发展。
研究结果发表在了4月1日的《Nature Medicine》上，科学家首次证明了大麻确实能减缓MS的发展速度，这将为全球大约250万疾病患者带来希望。
一组由伦敦大学神经免疫学教授David Baker领导的包括英国、欧洲、日本和美国科学家的国际研究小组以老鼠为模型，发现了一种大麻中的活性成分四氢大麻酚（THC）能显著的阻碍MS的发展和恶化。
大麻作用的机制在于激发身体内的大麻物质受体分子。研究小组之前曾报道过THC能通过受体CB1减轻某些疾病的症状，而且可以挽救受到疾病损伤的神经。但是他们并没有研究过大麻物质对于疾病的免疫方面的影响。
而现在的最新结果表明他们成功的区分了受体CB1和CB2在神经系统和T细胞上的作用，同时得到了它们对于控制中枢神经系统自体免疫方面的信息。CB1通过大脑神经表达，而非T细胞，它能激发和释放一种分子来阻碍MS发展，而与此同时T细胞激发CB2也起到类似作用。这表明类似大麻的药物可能阻碍导致疾病发展的自体免疫反应。
David Baker教授说：“应用CB1治疗存在某些风险，所以我们认为能通过CB2受体达到同样效果而不会带来副作用。”
译自：physorg.com
原始出处链接：http://www.physorg.com/news94743932.html
部分英文原文：
Nature Medicine，Published online: 1 April 2007; | doi:10.1038/nm1561
Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells
Katarzyna Maresz1, 11, Gareth Pryce2, 10, 11, Eugene D Ponomarev1, Giovanni Marsicano3, J Ludovic Croxford2, 4, Leah P Shriver1, 5, Catherine Ledent6, Xiaodong Cheng1, Erica J Carrier7, Monica K Mann1, 5, Gavin Giovannoni2, 10, Roger G Pertwee8, Takashi Yamamura4, Nancy E Buckley9, Cecilia J Hillard7, Beat Lutz3, David Baker2, 10, 11 & Bonnie N Dittel1, 5, 11
1 BloodCenter of Wisconsin, Blood Research Institute, Milwaukee, Wisconsin 53226, USA.
2 Department of Neuroinflammation, Institute of Neurology, University College London, London WC1N 1PJ, UK.
3 Department of Physiological Chemistry, Johannes Gutenberg-University Mainz, 55099 Mainz, Germany.
4 Department of Immunology, National Institute of Neuroscience, Tokyo 187-8502, Japan.
5 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
6 Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire, Université libre de Bruxelles, B-1070 Brussels, Belgium.
7 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
8 Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, UK.
9 Biological Sciences Department, California State Polytechnic University, Pomona, California 91768, USA.
10 Present address: Neuroimmunology Unit, Neuroscience Centre, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
11 These authors contributed equally to this work.
Correspondence should be addressed to Bonnie N Dittel bonnie.dittel@bcw.edu
The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB1 and CB2 cannabinoid receptors in regulating CNS autoimmunity. We found that CB1 receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB2 receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB2-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher rate of proliferation and increased production of inflammatory cytokines, resulting in severe clinical disease. Together, our results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.
