• David Panikashvili, Na'ama A Shein, Raphael Mechoulam, Victoria Trembovler, Ron Kohen, Alexander Alexandrovich, and Esther Shohami.
• Department of Pharmacology, Faculty of Medicine, School of Pharmacy, The Hebrew University School of Jerusalem, Jerusalem 91120, Israel.
• Neurobiol. Dis. 2006 May 1;22(2):257-64.

AbstractEndocannabinoids are involved in neuroprotection through numerous biochemical pathways. We have shown that the endocannabinoid 2-arachidonoyl glycerol (2-AG) is released in mouse brain after closed head injury (CHI), and treatment with exogenous 2-AG exerts neuroprotection via the central cannabinoid receptor CB1. This process involves inhibition of inflammatory signals that are mediated by activation of the transcription factor NF-kB. The present study was designed to examine the effect of 2-AG on the blood-brain barrier (BBB) and the possible inhibition of the early expression of proinflammatory cytokines, which are implicated in BBB disruption. We found that 2-AG decreased BBB permeability and inhibited the acute expression of the main proinflammatory cytokines: TNF-alpha, IL-1beta and IL-6. It also augmented the levels of endogenous antioxidants. We suggest that 2-AG exerts neuroprotection in part by inhibition of the early (1-4 h) inflammatory response and augmentation of the brain reducing power.

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