Transient Lack of Glucose but not O2 is Involved in Ischemic Postconditioning‐Induced Neuroprotection
Transient Lack of Glucose but not O2 is Involved in Ischemic Postconditioning‐Induced Neuroprotection
复制标题
DOI：
10.1111/cns.12033
复制
发表时间：
2013-01
影响因子：
5.5
通讯作者：
Yan-Ying Fan;Xiangnan Zhang;P. He;Zhe Shen;Yao Shen;Xiao-fen Wang;Weiwei Hu;Zhong Chen
中科院分区：
文献类型：
--
作者：
Yan-Ying Fan;Xiangnan Zhang;P. He;Zhe Shen;Yao Shen;Xiao-fen Wang;Weiwei Hu;Zhong Chen
脑缺血后处理是近年来出现的一种内源性神经保护机制。我们开始测试是否缺氧或葡萄糖剥夺（GD）将替代缺血后处理。
Cerebral ischemic postconditioning has emerged recently as a kind of endogenous strategy for neuroprotection. We set out to test whether hypoxia or glucose deprivation (GD) would substitute for ischemia in postconditioning.