INTERACTION BETWEEN DIETARY FLAVONOIDS AND THE BRAIN BARRIER





Kuresh Youdim, M. Zeeshan Qaiser, Catherine A. Rice-Evans & N. Joan Abbott

Antioxidant Research Group, Wolfson Centre for Age-Related Diseases, and Blood-Brain Barrier Group, Centre for Neuroscience Research, Guy's King's and St Thomas's School of Biomedical Sciences, King's College, London SE1 1UL



Recent studies highlight an exciting role with respect to the neuroprotective actions of dietary flavonoids. The mechanisms associated with flavonoid neuroprotection is complicated by the lack of information about their ability to enter the CNS. However, we have shown recently, using an in vitro blood-brain barrier (BBB) model (ECV304 co-cultured with C6 glioma cells) that flavonoids including their physiologically relevant metabolites exhibit high apparent permeability (Papp) across the brain endothelium. Using [3H] naringenin and [14C] quercetin as model substrates we have also shown in vivo, accumulation into 7 brain regions (cerebellum, cortex, hippocampus, hypothalamus, striatum, superior colliculus, and medulla). Total uptake (Kin ?L min-1 g-1) of naringenin was high in all regions studied, suggesting significant passive permeability. In contrast quercetin uptake was comparable to the P-glycoprotein (P-gp) efflux transporter substrate, colchicine. The potential influence of efflux transporters in mediating quercetin permeability in vivo, was studied by pre-administering animals with P-gp inhibitors PSC833 and GF120918 (10mg/kg). Only GF120918 significantly effected uptake. A closer examination of the role played by efflux transporters on flavonoid flux across the BBB was performed using MDCK-MDR1 and rat brain endothelial cells (RBE4) (both expressing functional P-gp). Our in vitro findings support observations in vivo, where flavonmoid accumulation was greatest in cells exposed to GF120918. In conclusion, these studies demonstrate that flavonoids are able to permeate the BBB but that some are possible substrates for efflux transporters, which limit their CNS bioavailability.




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