Abstract
The bradykinin B2 receptor (B2R) mediates many physiological processes such as hypotension, inflammation and blood-vessel permeability. Hypoxia/reoxygenation (H/R) induces neuronal cell apoptosis. It was found that B2R expression was enhanced in primary cultured cortical neurons after H/R treatment. Addition of bradykinin (BK) alleviated the neuronal damage from H/R. This protective effect of BK was inhibited by the B2R antagonist, HOE140, and the ERK1/2 antagonist, PD98059. The phosphorylation of ERK1/2 was increased under H/R, and the addition of BK enhanced this effect. These results indicate that B2R plays an important role in protecting neurons from damage induced by H/R and this effect may function through the ERK1/2 pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / physiology*
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Bradykinin / analogs & derivatives
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Bradykinin / pharmacology
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Bradykinin / therapeutic use
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Bradykinin B2 Receptor Antagonists
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Cell Hypoxia*
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Cells, Cultured
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Culture Media
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Flavonoids / pharmacology
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MAP Kinase Signaling System
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Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
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Mitogen-Activated Protein Kinase 1 / metabolism
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Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors
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Mitogen-Activated Protein Kinase 3 / metabolism
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Neurons / drug effects
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Neurons / physiology*
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Oxygen / metabolism*
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Phosphorylation / drug effects
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Protein Kinase Inhibitors / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptor, Bradykinin B2 / metabolism*
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Reperfusion Injury / physiopathology
Substances
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Bradykinin B2 Receptor Antagonists
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Culture Media
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Flavonoids
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Protein Kinase Inhibitors
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Receptor, Bradykinin B2
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icatibant
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Oxygen
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Bradykinin
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one