c-Jun N-terminal kinase activation in hippocampal CAI region was involved in ischemic injury

被引：55

作者：

Gu, ZL ^{[1
]}

Jiang, Q ^{[1
]}

Zhang, GY ^{[1
]}

机构：

[1] Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China

来源：

NEUROREPORT | 2001年 / 12卷 / 05期

关键词：

apoptosis; brain; c-Jun N-terminal kinase; hippocampus; ischemia; rat;

D O I：

10.1097/00001756-200104170-00006

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：897 / 900

页数：4

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