A Human Immortalized Cell-Based Blood–Brain Barrier Triculture Model: Development and Characterization as a Promising Tool for Drug−Brain Permeability Studies

2019 ◽  
Vol 16 (11) ◽  
pp. 4461-4471 ◽  
Author(s):  
Ryo Ito ◽  
Kenta Umehara ◽  
Shota Suzuki ◽  
Keita Kitamura ◽  
Ken-ichi Nunoya ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Model Development ◽  
Brain Barrier ◽  
Promising Tool ◽  
Blood Brain ◽  
Immortalized Cell ◽  
Permeability Studies

scholarly journals Identification of two immortalized cell lines, ECV304 and bEnd3, for in vitro permeability studies of blood-brain barrier

PLoS ONE ◽  
2017 ◽  
Vol 12 (10) ◽  
pp. e0187017 ◽  
Author(s):  
Shu Yang ◽  
Shenghui Mei ◽  
Hong Jin ◽  
Bin Zhu ◽  
Yue Tian ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Cell Lines ◽  
Brain Barrier ◽  
Immortalized Cell Lines ◽  
Blood Brain ◽  
Immortalized Cell ◽  
Permeability Studies

scholarly journals The Effects and Underlying Mechanisms of Cell Therapy on Blood-Brain Barrier Integrity After Ischemic Stroke

2020 ◽  
Vol 18 (12) ◽  
pp. 1213-1226
Author(s):  
Li Gao ◽  
Zhenghong Song ◽  
Jianhua Mi ◽  
Pinpin Hou ◽  
Chong Xie ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cell Therapy ◽  
Blood Brain Barrier ◽  
Current Knowledge ◽  
Brain Barrier ◽  
Neural Cells ◽  
Promising Tool ◽  
Cell Based Therapy ◽  
Blood Brain ◽  
Underlying Mechanisms

Ischemic stroke is one of the main causes of mortality and disability worldwide. However, efficient therapeutic strategies are still lacking. Stem/progenitor cell-based therapy, with its vigorous advantages, has emerged as a promising tool for the treatment of ischemic stroke. The mechanisms involve new neural cells and neuronal circuitry formation, antioxidation, inflammation alleviation, angiogenesis, and neurogenesis promotion. In the past decades, in-depth studies have suggested that cell therapy could promote vascular stabilization and decrease blood-brain barrier (BBB) leakage after ischemic stroke. However, the effects and underlying mechanisms on BBB integrity induced by the engrafted cells in ischemic stroke have not been reviewed yet. Herein, we will update the progress in research on the effects of cell therapy on BBB integrity after ischemic stroke and review the underlying mechanisms. First, we will present an overview of BBB dysfunction under the ischemic condition and cells engraftment for ischemic treatment. Then, we will summarize and discuss the current knowledge about the effects and underlying mechanisms of cell therapy on BBB integrity after ischemic stroke. In particular, we will review the most recent studies in regard to the relationship between cell therapy and BBB in tissue plasminogen activator (t-PA)-mediated therapy and diabetic stroke.

scholarly journals Flavonoid transport across RBE4 cells: A blood-brain barrier model

2010 ◽  
Vol 15 (2) ◽  
Author(s):  
Ana Faria ◽  
Diogo Pestana ◽  
Diana Teixeira ◽  
Joana Azevedo ◽  
Victor Freitas ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Cerebrovascular Diseases ◽  
Brain Barrier ◽  
Array Detector ◽  
Dependent Manner ◽  
Blood Brain ◽  
Parkinson’S Diseases ◽  
Blood Brain Barrier Model ◽  
Immortalized Cell ◽  
Barrier Model

AbstractThere is a growing interest in dietary therapeutic strategies to combat oxidative stress-induced damage to the Central Nervous System (CNS), which is associated with a number of pathophysiological processes, including Alzheimer’s and Parkinson’s diseases and cerebrovascular diseases. Identifying the mechanisms associated with phenolic neuroprotection has been delayed by the lack of information concerning the ability of these compounds to enter the CNS. The aim of this study was to evaluate the transmembrane transport of flavonoids across RBE-4 cells (an immortalized cell line of rat cerebral capillary endothelial cells) and the effect of ethanol on this transport. The detection and quantification of all of the phenolic compounds in the studied samples (basolateral media) was performed using a HPLC-DAD (Diode Array Detector). All of the tested flavonoids (catechin, quercetin and cyanidin-3-glucoside) passed across the RBE-4 cells in a time-dependent manner. This transport was not influenced by the presence of 0.1% ethanol. In conclusion, the tested flavonoids were capable of crossing this blood-brain barrier model.

Permeability Studies on In Vitro Blood–Brain Barrier Models: Physiology, Pathology, and Pharmacology

2005 ◽  
Vol 25 (1) ◽  
pp. 59-127 ◽  
Author(s):  
Mária A. Deli ◽  
Csongor S. Ábrahám ◽  
Yasufumi Kataoka ◽  
Masami Niwa
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Permeability Studies

scholarly journals Hyperosmolar Opening of the Blood-Brain Barrier in the Energy-Depleted Rat Brain. Part 1. Permeability Studies

1988 ◽  
Vol 8 (1) ◽  
pp. 9-15 ◽  
Author(s):  
J. Greenwood ◽  
P. J. Luthert ◽  
O. E. Pratt ◽  
P. L. Lantos
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Surrounding Tissue ◽  
Control Value ◽  
A Value ◽  
Blood Brain ◽  
Hyperosmolar Solutions ◽  
Barrier Opening ◽  
Permeability Studies ◽  
The Brain

A simple saline perfusion system was used to investigate the effects of hyperosmolar solutions of arabinose and mannitol upon the permeability of the blood-brain barrier. The small, polar molecule [14C]mannitol and the larger, visual marker Evans blue were used as indicators of barrier integrity in the perfused energydepleted brain. One-minute perfusion of hyperosmolar solutions consistently opened the barrier suggesting that the mechanism of osmotic barrier opening is independent of energy-producing metabolism. The accumulation of radiolabel in the brain was expressed as the ratio of tissue to perfusate radioactivity ( Rt/ Rp) and, for cerebrum, this increased from a control value of 0.0022 ± 0.0007 (mean ± SEM; n = 4) to a value of 0.0124 ± 0.0008 (n = 4) following 0.9 M arabinose and to 0.0495 ± 0.0072 (n = 4) following 1.8 M arabinose. There was a significant reduction of water content of hyperosmolar perfused brains. These findings support the hypothesis that osmotic barrier opening is the result of the passive shrinkage of endothelial cells and the surrounding tissue.

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