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It is well established fact regarding various in vitro blood-brain
barrier drug transport models that down regulation of transport
conditions is a major hurdle. For example: In bovine cultured brain
capillary endothelial cells the expression of glucose transporter
(CGLUT1) is suppressed 150 fold in comparision to the in vivo level. In
conditionally immortalized TR-BBB cells, the transport activity for
3-O-methyl-D-glucose(3-OMG), specific substrate for GLUT1 in these
cells is estimated to be 20 % for that in vivo BBB measured by means of
the Brain uptake Index and/or Brain efflux index methods.
Basing by this fact, is the same problem of downregulation of transport
function carry sense with Caco-2 cell cultures? If so, how it can be
averted. Are there any reports of such a phenomenon in Caco-2 cell
cultures published ??
Ravi Kanth Bhamidipati
Dept.of Drug Metabolism and Pharmacokinetics
Discovery Research Division
Dr.Reddy's Laboratories Ltd.
Bollaram Road , Miyapur
Hyderabad - 500 049
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