NMDA blockade attenuates caspase-3 activation and DNA fragmentation after neonatal hypoxia-ischemia

被引：38

作者：

Puka-Sundvall, M

Hallin, U

Zhu, CL

Wang, XY

Karlsson, JO

Blomgren, K

Hagberg, H

机构：

[1] Univ Gothenburg, Dept Anat & Cell Biol, S-40530 Gothenburg, Sweden

[2] Univ Gothenburg, Dept Physiol, S-40530 Gothenburg, Sweden

[3] Univ Gothenburg, Dept Obstet & Gynecol, S-40530 Gothenburg, Sweden

[4] Univ Gothenburg, Dept Physiol, Perinatal Ctr, S-40530 Gothenburg, Sweden

来源：

NEUROREPORT | 2000年 / 11卷 / 13期

关键词：

apoptosis; brain damage; caspase-3; hypoxia-ischemia; NMDA receptor; neonatal;

D O I：

10.1097/00001756-200009110-00002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The aim was to study the effects of an NMDA receptor antagonist on caspase-3 activation and DNA fragmentation after hypoxia-ischemia (HI) in 7-day-old rats. Animals were treated with vehicle or MK-801 (0.5mg/kg) directly after HI and sacrificed 8, 24 or 72 h later. MK-801 reduced injury (by 53%), cells positive for active caspase-3 (by 39%) and DNA fragmentation (by 79%) in the cerebral cortex. Furthermore, MK-801 significantly decreased caspase-3 activity, and Western blots revealed a tendency towards decreased proteolytic cleavage of the caspase-3 preform. The data imply that NMDA receptors are involved in the activation of apoptotic processes in the immature brain after HI. NeuroReport 11:2833-2836 (C) 2000 Lippincott Williams & Wilkins.

引用

页码：2833 / 2836

页数：4

共 24 条

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