Cannabinoids and experimental models of multiple sclerosis

被引:28
作者
Kubajewska, Ilona [1 ]
Constantinescu, Cris S. [1 ]
机构
[1] Univ Nottingham, Queens Med Ctr, Div Clin Neurol, Nottingham NG7 2UH, England
关键词
Cannabinoids; Cannabinoid receptors; Cytokines; Experimental autoimmune; encephalomyelitis; Inflammation; Neuroprotection; Multiple sclerosis; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; ENCEPHALITOGENIC T-CELLS; CENTRAL-NERVOUS-SYSTEM; SITU HYBRIDIZATION HISTOCHEMISTRY; RECEPTOR MESSENGER-RNA; ENDOCANNABINOID SYSTEM; RAT-BRAIN; IMMUNE-SYSTEM; CB1; RECEPTORS;
D O I
10.1016/j.imbio.2009.08.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The inflammatory response is a hallmark in the development of autoimmune-mediated neurodegenerative diseases of the central nervous system (CNS). Research on these pathological phenomena is being extensively undertaken and experimental autoimmune encephalomyelitis (EAE) serves as a valuable animal model. Studies from this model have generated interesting insights into biological effects of cannabinoids and may, at least to a certain extent, reflect the cannabinoid-mediated protective mechanisms also in human diseases with similar characteristics, such as multiple sclerosis (MS). Cannabinoids are involved in regulation of the immune system. These effects comprise modulation of inflammatory reaction through components of the innate and adaptive immune responses. Cannabinoids also confer neuroprotection and assist neuroregeneration, thus maintaining a balance within the delicate CNS microenvironment and restoring function following pathological condition, commonly driven by neuroinfiammation. Continued studies of cannabinoid actions in EAE pathogenesis should be beneficial for the better understanding of the mechanisms governing such a vast array of physiological effects and in development of new therapeutic strategies for the treatment of human neuroinflammatory and neurodegenerative diseases. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:647 / 657
页数:11
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