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• W2022642913 startingPage "1686" @default.
• W2022642913 abstract "Cytosolic phospholipase A 2 (cPLA 2 ) is a key enzyme that mediates arachidonic acid metabolism, which causes cerebral ischemia-induced oxidative injury, blood—brain barrier (BBB) dysfunction, and edema. Recent reports have shown that p38 mitogen—activated protein kinase (MAPK) is related to phosphorylation and activation of cPLA 2 and release of arachidonic acid. However, involvement of the p38 MAPK pathway in cPLA 2 activation and of reactive oxygen species in expression of p38 MAPK/cPLA 2 after ischemia—reperfusion injury in the brain remains unclear. To address these issues, we used a model of transient focal cerebral ischemia (tFCI) in rats. Western blot analysis showed a significant increase in expression of phospho-p38 MAPK and phospho-cPLA 2 in rat brain cortex after tFCI. Activity assays showed that both p38 MAPK and cPLA 2 activation markedly increased 1 day after reperfusion. Intraventricular administration of SB203580 significantly suppressed activation and phosphorylation of cPLA 2 and attenuated BBB extravasation and subsequent edema. Moreover, overexpression of copper/zinc-superoxide dismutase remarkably diminished activation and phosphorylation of both p38 MAPK and cPLA 2 after reperfusion. These findings suggest that the p38 MAPK/cPLA 2 pathway may promote BBB disruption with secondary vasogenic edema and that superoxide anions can stimulate this pathway after ischemia—reperfusion injury." @default.
• W2022642913 created "2016-06-24" @default.
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• W2022642913 date "2008-06-11" @default.
• W2022642913 modified "2023-10-16" @default.
• W2022642913 title "Role of the p38 Mitogen-Activated Protein Kinase/Cytosolic Phospholipase A₂ Signaling Pathway in Blood—Brain Barrier Disruption after Focal Cerebral Ischemia and Reperfusion" @default.
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• W2022642913 doi "https://doi.org/10.1038/jcbfm.2008.60" @default.
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