AI Article Synopsis
- Endocannabinoid 2-arachidonoyl glycerol (2-AG) shows neuroprotective effects following brain injury in mice by activating the CB1 receptor and inhibiting inflammatory responses.
- 2-AG treatment reduces blood-brain barrier (BBB) permeability and lowers levels of proinflammatory cytokines like TNF-alpha, IL-1beta, and IL-6 after a closed head injury.
- Additionally, 2-AG increases endogenous antioxidants, suggesting it helps protect the brain by both reducing inflammation and boosting the brain's defense mechanisms soon after injury.
Article 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-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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| http://dx.doi.org/10.1016/j.nbd.2005.11.004 | DOI Listing |
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