Jacob Bell
New Member
David Panikashvili, Na'ama A Shein, Raphael Mechoulam, Victoria Trembovler, Ron Kohen, Alexander Alexandrovich, Esther Shohami
Department of Pharmacology, Faculty of Medicine, School of Pharmacy, The Hebrew University School of Jerusalem, Jerusalem 91120, Israel; Medicinal Chemistry and Natural Products, The Hebrew University School of Pharmacy, Faculty of Medicine, Jerusalem, Israel.
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 CB(1). 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.
Keywords: endocannabinoid; bbb; close head; head injury; proinflammatory cytokine; after close; cytokine; proinflammatory; blood-brain; blood-brain barrier; injury; barrier after; inhibit mrna; head; neuroprotection.
Source: The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines
Department of Pharmacology, Faculty of Medicine, School of Pharmacy, The Hebrew University School of Jerusalem, Jerusalem 91120, Israel; Medicinal Chemistry and Natural Products, The Hebrew University School of Pharmacy, Faculty of Medicine, Jerusalem, Israel.
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 CB(1). 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.
Keywords: endocannabinoid; bbb; close head; head injury; proinflammatory cytokine; after close; cytokine; proinflammatory; blood-brain; blood-brain barrier; injury; barrier after; inhibit mrna; head; neuroprotection.
Source: The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines
