scholarly journals P-glycoprotein in the blood-brain barrier of mice influences the brain penetration and pharmacological activity of many drugs.

1996 ◽  
Vol 97 (11) ◽  
pp. 2517-2524 ◽  
Author(s):  
A H Schinkel ◽  
E Wagenaar ◽  
C A Mol ◽  
L van Deemter
Keyword(s):  
Blood Brain Barrier ◽  
Pharmacological Activity ◽  
Brain Barrier ◽  
Brain Penetration ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

scholarly journals Nonlinear accumulation in the brain of the new taxoid TXD258 following saturation of P-glycoprotein at the blood-brain barrier in mice and rats

2003 ◽  
Vol 138 (7) ◽  
pp. 1367-1375 ◽  
Author(s):  
Salvatore Cisternino ◽  
Fanchon Bourasset ◽  
Yves Archimbaud ◽  
Dorothée Sémiond ◽  
Gérard Sanderink ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

Drug transport to the brain: key roles for the efflux pump P-glycoprotein in the blood–brain barrier

2002 ◽  
Vol 38 (6) ◽  
pp. 339-348 ◽  
Author(s):  
Michel Demeule ◽  
Anthony Régina ◽  
Julie Jodoin ◽  
Alain Laplante ◽  
Claude Dagenais ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Drug Transport ◽  
Efflux Pump ◽  
Brain Barrier ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

Inhibition of P-glycoprotein Activity at the Primate Blood-Brain Barrier Increases the Distribution of Nelfinavir into the Brain but Not into the Cerebrospinal Fluid

2007 ◽  
Vol 35 (9) ◽  
pp. 1459-1462 ◽  
Author(s):  
Amal Kaddoumi ◽  
Sung-Up Choi ◽  
Loren Kinman ◽  
Dale Whittington ◽  
Che-Chung Tsai ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

P2-347: Absence of MDR-1 P-glycoprotein at the blood-brain barrier increased the passage of blood-borne exogenous Aβ peptides across the BBB into the brain

2010 ◽  
Vol 6 ◽  
pp. S415-S416
Author(s):  
Wandong Zhang ◽  
Huaqi Xiong ◽  
Shanshan Shen ◽  
Aimee Jones ◽  
Peilin Huang ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Aβ Peptides ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain ◽  
Mdr 1

scholarly journals Toward Eradicating HIV Reservoirs in the Brain: Inhibiting P-Glycoprotein at the Blood–Brain Barrier with Prodrug Abacavir Dimers

2011 ◽  
Vol 134 (6) ◽  
pp. 2976-2980 ◽  
Author(s):  
Hilda A. Namanja ◽  
Dana Emmert ◽  
David A. Davis ◽  
Christopher Campos ◽  
David S. Miller ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Hiv Reservoirs ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

scholarly journals Norfloxacin Blood-Brain Barrier Transport in Rats Is Not Affected by Probenecid Coadministration

2006 ◽  
Vol 50 (1) ◽  
pp. 371-373 ◽  
Author(s):  
Sandrine Marchand ◽  
Anna Forsell ◽  
Marylore Chenel ◽  
Emmanuelle Comets ◽  
Isabelle Lamarche ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Penetration ◽  
Penetration Factor ◽  
Blood Brain ◽  
Drug Concentrations ◽  
The Brain

ABSTRACT The effect of probenecid (PRO) on norfloxacin (NOR) blood-brain barrier transport was investigated with rats by microdialysis. Maximum brain drug concentrations were rapidly attained, and the brain penetration factor was close to 5% in the absence and presence of PRO. In conclusion, PRO has no effect on NOR blood-brain barrier transport.

scholarly journals Functional activity of p-glycoprotein in blood-brain barrier during experimental par-kinson's syndrome

2019 ◽  
Vol 27 (2) ◽  
pp. 150-159
Author(s):  
Ivan V. Chernykh ◽  
Aleksey V. Shchulkin ◽  
Pavel Yu. Mylnikov ◽  
Maria V. Gatsanoga ◽  
Maria M. Gradinar ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Intravenous Administration ◽  
Functional Activity ◽  
Brain Barrier ◽  
Renal Tubules ◽  
Parkinson's Syndrome ◽  
Parkinson’S Syndrome ◽  
P Glycoprotein ◽  
Blood Brain ◽  
The Brain

Background. P-glycoprotein (Pgp, ABCB1-protein) is a membrane transporter with broad substrate specificity that is localized in hepatocytes, enterocytes, epithelial renal tubules, and also in tissue barriers, including blood-brain barrier (BBB). Increased Pgp activity in BBB is one of the reasons for the pharmacoresistance of a number of CNS diseases. Aim. Analysis of Pgp functional activity in BBB during experimental Parkinson's syndrome. Materials and Methods. The work was performed on 90 Wistar rats, divided into 3 series (n=30 in each). The 1 series (control) was subcutaneously injected sunflower oil once a day for 7 days, and Pgp activity in BBB was assessed on the 8th day. The 2 and 3 series (pathology control) - were administered rotenone at a dose of 2.5 mg/kg once a day for 7 and 28 days respectively to simulate parkin-sonism. At the end of the experiment Pgp activity was estimated. To confirm Parkinson's syndrome, in addition to the clinical picture, level of dopamine in midbrain and striatum was determined using enzyme-linked immunosorbent assay. Pgp functional activity in BBB was assessed by the degree of penetration of its marker substrate fexofenadine into the brain after its intravenous administration at a dose of 10 mg/kg. The content of fexofenadine in the blood plasma and in brain tissue was estimated by the area under pharmacokinetic curve of the substance (in the blood or brain tissues) - AUC0-t(plasma) or AUC0-t(brain) respectively. To assess the BBB permeability the ratio AUC0-t(brain) / AUC0-t(plasma) was calculated. Results. Rotenone administration led to the development of parkinsonism typical picture: muscle stiffness, hypokinesia, gait instability. There was a decrease in dopamine level in the striatum after 7 days by 69.6% (p=0.095), after 28 days - by 93.9% (p=0.008), in midbrain - by 72.7% (p=0.095) and 68.7% (p=0.032) respectively. Fexofenadine AUC0-t(plasma) and AUC0-t(brain) after its intravenous administration to control rats were 266.2 (246.4; 285.6) μg/ml*min and 5.9 (5.8;6.6) µg/g*min respectively, AUC0-t(brain) /AUC0-t(plasma) - 0.020 (0.019; 0.022). When rotenone was for 7 days administered - fexofenadine AUC0-t(brain) increased 2.02 times (p=0.0163), AUC0-t(brain) / AUC0-t(plasma) - 2.4 times (p=0.0283). 28 days administration of rotenone led to augmentation of AUC0-t(brain) of fexofenadine by 1.75 times (p=0.0283), AUC0-t(brain) / AUC0-t(plasma) - by 2.27 times (p=0.0163). Conclusions. The development of Parkinson’s syndrome, caused by the administration of rotenone, inhibits Pgp functional activity in BBB, which is confirmed by the accumulation in the brain marker substrate of the transporter - fexofenadine.

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