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

2004; Elsevier BV; Volume: 1016; Issue: 2 Linguagem: Inglês

10.1016/j.brainres.2004.05.017

1872-6240

Vittorio Colangelo, William C. Gordon, Pranab K. Mukherjee, Pankaj Trivedi, Paulo Ottino,

Traditional Chinese Medicine Analysis

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.