Sayer Ji
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Abstract Title:

Cannabidiol inhibits pathogenic T cells, decreases spinal microglial activation and ameliorates multiple sclerosis-like disease in C57BL/6 mice.

Abstract Source:

Br J Pharmacol. 2011 Mar 30. Epub 2011 Mar 30. PMID: 21449980

Abstract Author(s):

Ewa Kozela, Nirit Lev, Nathali Kaushansky, Raya Eilam, Neta Rimmerman, Rivka Levy, Avraham Ben-Nun, Ana Juknat, Zvi Vogel

Article Affiliation:

The Dr. Miriam and Sheldon G. Adelson Center for the Biology of Addictive Diseases, Physiology and Pharmacology Department, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; Neurology Department, Rabin Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; Immunology Department, Histology Department, Neurobiology Department, Weizmann Institute of Science, Rehovot, Israel.

Abstract:

Objective: Cannabis extracts and several cannabinoids, have been shown to exert broad anti-inflammatory activities including in experimental models of inflammatory CNS degenerative diseases. The clinical future of many cannabinoids is limited due to their psychotropic effects. However, phytocannabinoids like cannabidiol (CBD), void of psychoactive activity, have a potential to be safe and effective alternatives for alleviating neuroinflammation and neurodegeneration. Materials and methods: We studied the effects of CBD, in myelin oligodendrocyte glycoprotein (MOG)-induced EAE model of multiple sclerosis in C57BL/6 mice. Using immunocytochemistry and cell proliferation assays we evaluated the effects of CBD on microglial activation in MOG-immunized animals and CBD effect in MOG-specific T cell proliferation. Results: We observed that CBD administration during disease onset ameliorates the severity of EAE clinical signs. The alleviation of EAE severity by CBD was accompanied by diminished axonal damage and inflammation as well as microglial activation and T cell recruitment in the spinal cord of MOG-injected mice. Moreover, CBD inhibited MOG-induced T cell proliferation in vitro at both low and high concentrations of myelin antigen. This effect was not mediated via the known cannabinoid receptors, CB(1) and CB(2) . Conclusions: CBD, a non psychoactive cannabinoid, ameliorates clinical signs of MOG-immunized EAE mice. Suppression of microglial activity and T cell proliferation by CBD seems to contribute to these beneficial effects.

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Sayer Ji
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