Downregulation of COX-2 and JNK expression after induction of ischemic tolerance in the gerbil brain

Brain Research
Vittorio ColangeloPaulo Ottino

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.

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Citations

Jun 21, 2005·European Journal of Pharmacology·Tania F GendronPaul Morley
Jun 18, 2015·Molecular Neurobiology·N Thushara VijayakumarG K Rajanikant
Sep 3, 2011·Surgical Neurology International·Russell L Blaylock, Joseph Maroon
Apr 9, 2020·Frontiers in Cellular Neuroscience·Denisa Belov KirdajovaMiroslava Anderova

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