scholarly journals Edaravone-Encapsulated Agonistic Micelles Rescue Ischemic Brain Tissue by Tuning Blood-Brain Barrier Permeability

Theranostics ◽  
2017 ◽  
Vol 7 (4) ◽  
pp. 884-898 ◽  
Author(s):  
Qu Jin ◽  
Yu Cai ◽  
Sihan Li ◽  
Haoran Liu ◽  
Xingyu Zhou ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Ischemic Brain ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Ischemic Brain Tissue

scholarly journals Dimethylthiourea Reduces Ischemic Brain Edema without Affecting Cerebral Blood Flow

1990 ◽  
Vol 10 (3) ◽  
pp. 352-357 ◽  
Author(s):  
Dean Martz ◽  
Mary Beer ◽  
A. Lorris Betz
Keyword(s):  
Brain Edema ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Radical Scavenger ◽  
Ischemic Brain ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Ischemic Brain Edema

Oxygen free radicals have been implicated as mediators of tissue damage in ischemic brain. We previously demonstrated that the hydroxyl radical scavenger 1,3-dimethyl-2-thiourea (DMTU) reduces infarct size after middle cerebral artery occlusion (MCAO) in rats. The present study was undertaken to determine whether this protection results from a preservation of the CBF. Adult male Sprague-Dawley rats were treated with DMTU (750 mg/kg i.p.) or saline vehicle 1 h before right MCAO. One-half, 4, or 24 h after MCAO, animals were killed and samples were taken from the central, intermediate, and outer zones of the MCA distribution of each cortical mantle. Separate groups of animals were used to analyze these samples for water content (wet and dry weight), CBF ([14C]butanol), or blood–brain barrier permeability ([3H]α-aminoisobutyric acid). CBF was reduced in a graded fashion in the ischemic cortex: 0.169 ± 0.020, 0.261 ± 0.017, and 0.435 ± 0.023 ml/g/min (mean ± SEM, n = 8) after 4 h in the central, intermediate, and outer zones, respectively. Brain edema was present in a similar pattern, while blood–brain barrier permeability remained normal. Treatment with DMTU significantly reduced brain edema in the central and intermediate zones at both 4 and 24 h. However, CBF in the DMTU-treated animals was identical to that of the vehicle-treated animals. These results suggest that hydroxyl radicals play a role in the development of ischemic brain edema, but the mechanism does not appear to involve a direct effect on CBF.

scholarly journals Modulation of Blood–Brain Barrier Permeability by Activating Adenosine A2 Receptors in Oncological Treatment

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 633
Author(s):  
Kamila Wala ◽  
Wojciech Szlasa ◽  
Jolanta Saczko ◽  
Julia Rudno-Rudzińska ◽  
Julita Kulbacka
Keyword(s):  
Brain Tumors ◽  
Brain Tissue ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Primary Brain Tumors ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Bbb Permeability

The blood–brain barrier (BBB) plays an important protective role in the central nervous system and maintains its homeostasis. It regulates transport into brain tissue and protects neurons against the toxic effects of substances circulating in the blood. However, in the case of neurological diseases or primary brain tumors, i.e., gliomas, the higher permeability of the blood-derived substances in the brain tissue is necessary. Currently applied methods of treatment for the primary brain neoplasms include surgical removal of the tumor, radiation therapy, and chemotherapy. Despite the abovementioned treatment methods, the prognosis of primary brain tumors remains bad. Moreover, chemotherapy options seem to be limited due to low drug penetration into the cancerous tissue. Modulation of the blood–brain barrier permeability may contribute to an increase in the concentration of the drug in the CNS and thus increase the effectiveness of therapy. Interestingly, endothelial cells in cerebral vessels are characterized by the presence of adenosine 2A receptors (A2AR). It has been shown that substances affecting these receptors regulate the permeability of the BBB. The mechanism of increasing the BBB permeability by A2AR agonists is the actin-cytoskeletal reorganization and acting on the tight junctions. In this case, the A2AR seems to be a promising therapy target. This article aims to assess the possibility of increasing the BBB permeability through A2AR agonists to increase the effectiveness of chemotherapy and to improve the results of cancer therapy.

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