科學(xué)家最新研究發(fā)現(xiàn),，大麻中的化學(xué)物質(zhì)能用于治療人類(lèi)多發(fā)性硬化癥（MS），這一發(fā)現(xiàn)能大大提高治療的效果，因?yàn)榇舐槲镔|(zhì)不但能減少神經(jīng)損傷以及異常神經(jīng)沖動(dòng)產(chǎn)生，更重要的是它能阻止疾病的進(jìn)一步發(fā)展。
研究結(jié)果發(fā)表在了4月1日的《Nature Medicine》上,，科學(xué)家首次證明了大麻確實(shí)能減緩MS的發(fā)展速度，這將為全球大約250萬(wàn)疾病患者帶來(lái)希望,。
一組由倫敦大學(xué)神經(jīng)免疫學(xué)教授David Baker領(lǐng)導(dǎo)的包括英國(guó),、歐洲、日本和美國(guó)科學(xué)家的國(guó)際研究小組以老鼠為模型,，發(fā)現(xiàn)了一種大麻中的活性成分四氫大麻酚（THC）能顯著的阻礙MS的發(fā)展和惡化,。
大麻作用的機(jī)制在于激發(fā)身體內(nèi)的大麻物質(zhì)受體分子。研究小組之前曾報(bào)道過(guò)THC能通過(guò)受體CB1減輕某些疾病的癥狀,，而且可以挽救受到疾病損傷的神經(jīng),。但是他們并沒(méi)有研究過(guò)大麻物質(zhì)對(duì)于疾病的免疫方面的影響。
而現(xiàn)在的最新結(jié)果表明他們成功的區(qū)分了受體CB1和CB2在神經(jīng)系統(tǒng)和T細(xì)胞上的作用,，同時(shí)得到了它們對(duì)于控制中樞神經(jīng)系統(tǒng)自體免疫方面的信息,。CB1通過(guò)大腦神經(jīng)表達(dá)，而非T細(xì)胞,，它能激發(fā)和釋放一種分子來(lái)阻礙MS發(fā)展,，而與此同時(shí)T細(xì)胞激發(fā)CB2也起到類(lèi)似作用。這表明類(lèi)似大麻的藥物可能阻礙導(dǎo)致疾病發(fā)展的自體免疫反應(yīng)。
David Baker教授說(shuō)：“應(yīng)用CB1治療存在某些風(fēng)險(xiǎn),，所以我們認(rèn)為能通過(guò)CB2受體達(dá)到同樣效果而不會(huì)帶來(lái)副作用,。”
譯自：physorg.com
原始出處鏈接：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 [email protected]
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.
