期刊
NEUROREPORT
卷 12, 期 5, 页码 897-900出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200104170-00006
关键词
apoptosis; brain; c-Jun N-terminal kinase; hippocampus; ischemia; rat
To clarify the role of c-Jun N-terminal kinase (JNK) activation in brain ischemia, temporospatial alteration of active (diphosphorylated) JNK1/2 immunoreactivity in hippocampus after brain ischemia in rat was investigated. Western immunoblot study showed that JNK1/2 diphosphorylation level was increased biphasically in CA1 but not CA3/dentate gyrus (DG) after 10 min of ischemia. Cerebral ventricular infusion of JNK1/2 antisense oligonucleotides not only significantly decreased JNK1/2 protein expression and the activation level but also significantly decreased CA1 pyramidal cell death (demonstrated by cresyl violet staining) and DNA fragmentation (demonstrated by in situ end-labeling of DNA). These results suggest that JNK1/2 were selectively activated and involved in the selective cell death in hippocampal CA1 subfield after cerebral ischemia. NeuroReport 12:897-900 (C) 2001 Lippincott Williams & Wilkins.
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