Abstract
Endocannabinoids 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-α, IL-1β 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.
Original language | American English |
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Pages (from-to) | 257-264 |
Number of pages | 8 |
Journal | Neurobiology of Disease |
Volume | 22 |
Issue number | 2 |
DOIs | |
State | Published - May 2006 |
Keywords
- BBB integrity
- Cytokines
- Endocannabinoids
- Inflammation
- Neuroprotection
- Reactive oxygen species
- Traumatic brain injury