Cerebral protection by hypoxic preconditioning in a murine model of focal ischemia-reperfusion
Cerebral protection by hypoxic preconditioning in a murine model of focal ischemia-reperfusion
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DOI：
10.1097/00001756-200106130-00030
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发表时间：
2001-06-13
期刊：
影响因子：
1.7
通讯作者：
Gidday, JM
中科院分区：
文献类型：
--
作者：
Miller, BA;Perez, RS;Gidday, JM
在所谓的缺血预适应过程中，亚致死期的缺氧或缺血可诱导适应性机制，以保护其免受随后的致命性缺血损伤。在本研究中，我们使用几种常见的成年小鼠品系建立了一种小鼠脑预适应模型。线栓法制备大鼠大脑中动脉短暂局灶性闭塞模型，造模前48h暴露于亚致死性低氧(11%氧气，持续2 h)，24 h后用TTC染色评价损伤程度。C57B1/6、129SvEv和Swiss-Webster ND4小鼠的脑梗塞体积在低氧预适应动物中分别减少了46%、58%和%。这种非侵入性的小鼠缺血耐受模型应该有助于利用转基因和基因敲除小鼠阐明这种保护的分子基础。《神经报告》12：1663-1669(C)2001 Lippincott Williams&Wilkins.
Sublethal periods of hypoxia or ischemia can induce adaptive mechanisms to protect against subsequent lethal ischemic insults in a process known as ischemic preconditioning. In the present study, we developed a murine model of cerebral preconditioning using several common strains of adult mice. Animals were exposed to sublethal hypoxia (11% oxygen for 2 h) 48 h prior to a 90 min period of transient focal middle cerebral artery occlusion, induced by an intraluminal filament; injury was assessed 24 h later by TTC staining. Infarct volume in hypoxia-preconditioned animals was reduced 46%, 58%, and 64% in C57B1/6, 129SvEv, and Swiss-Webster ND4 mice relative to their respective untreated controls. This noninvasive murine model of ischemic tolerance should be useful for elucidating the molecular basis of this protection using transgenic and knockout mice. NeuroReport 12:1663-1669 (C) 2001 Lippincott Williams & Wilkins.