RESVERATROL PREVENTS BRAIN EDEMA, BLOOD‐BRAIN BARRIER PERMEABILITY AND ALTERED AQUAPORIN PROFILE IN AUTISM ANIMAL MODEL

2021 ◽  
Author(s):  
Iohanna Deckmann ◽  
Júlio Santos‐Terra ◽  
Mellanie Fontes‐Dutra ◽  
Marília Körbes‐Rockenbach ◽  
Guilherme Bauer‐Negrini ◽  
...  
Keyword(s):  
Animal Model ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

scholarly journals Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

2010 ◽  
Vol 10 ◽  
pp. 1180-1191 ◽  
Author(s):  
Fatemeh Mohagheghi ◽  
Mohammad Reza Bigdeli ◽  
Bahram Rasoulian ◽  
Ali Asghar Zeinanloo ◽  
Ali Khoshbaten
Keyword(s):  
Brain Edema ◽  
Blood Brain Barrier ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Virgin Olive Oil ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in anin vivostudy of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control) received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively). After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO). After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p< 0.05), and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p< 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.

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.

Sign in / Sign up

Export Citation Format

Share Document