Abstract
The response of the inducible isoform of the prostaglandin H2 synthase (COX-2) and the c-Jun N-terminal kinase (JNK) in post-ischemic neuronal damage was assessed in a model of ischemic tolerance in Mongolian Gerbils. After a single 6-min bilateral carotid occlusion, histological damage was evident in the CA1 region of hippocampus, correlated with a high expression of JNK and COX-2 mRNA. However, in the group of animals with a 2-min ischemia and the tolerance group, in which a 2-min bilateral carotid occlusion was followed 3 days later by a 6-min ischemia, no hippocampal or cortical damage was detected. Accordingly, the JNK and COX-2 mRNA levels remained unaffected. We suggest that the level of JNK and COX-2 expression may determine the outcome as either post-ischemic cell death or tolerance.
Publication types
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Comparative Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Western / methods
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Cell Count / methods
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Cell Death / physiology
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Cyclooxygenase 2
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Disease Models, Animal
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Female
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Gene Expression Regulation*
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Gerbillinae
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In Situ Nick-End Labeling / methods
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Ischemic Attack, Transient / genetics
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Ischemic Attack, Transient / metabolism*
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Ischemic Preconditioning*
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Isoenzymes / genetics
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Isoenzymes / metabolism*
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases / genetics
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Mitogen-Activated Protein Kinases / metabolism*
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Prostaglandin-Endoperoxide Synthases / genetics
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Prostaglandin-Endoperoxide Synthases / metabolism*
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction / methods
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Time Factors
Substances
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Isoenzymes
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RNA, Messenger
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Cyclooxygenase 2
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Prostaglandin-Endoperoxide Synthases
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases