scholarly journals MicroRNA‐130a regulates cerebral ischemia–induced blood–brain barrier permeability by targeting Homeobox A5

2018 ◽  
Vol 32 (2) ◽  
pp. 935-944 ◽  
Author(s):  
Yong Wang ◽  
Meng‐Die Wang ◽  
Yuan‐Peng Xia ◽  
Yuan Gao ◽  
Yi‐Yi Zhu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Superior Neuroprotective Efficacy of a Novel Antioxidant (U-101033E) With Improved Blood-Brain Barrier Permeability in Focal Cerebral Ischemia

Stroke ◽  
1997 ◽  
Vol 28 (10) ◽  
pp. 2018-2024 ◽  
Author(s):  
Robert Schmid-Elsaesser ◽  
Stefan Zausinger ◽  
Edwin Hungerhuber ◽  
Nikolaus Plesnila ◽  
Alexander Baethmann ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Neuroprotective Efficacy

Oxygen radicals in cerebral ischemia

1992 ◽  
Vol 263 (5) ◽  
pp. H1356-H1362 ◽  
Author(s):  
C. W. Nelson ◽  
E. P. Wei ◽  
J. T. Povlishock ◽  
H. A. Kontos ◽  
M. A. Moskowitz
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Superoxide Production ◽  
Brain Barrier ◽  
Early Reperfusion ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Vasodilator Response ◽  
Blood Brain ◽  
Brain Barrier Permeability

Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.

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