Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3 beta through the PI3K/Akt survival pathway
Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3 beta through the PI3K/Akt survival pathway
复制标题
七氟烷延迟后处理诱导的神经保护作用可归因于通过 PI3K/Akt 存活途径增加线粒体 GSK-3 β 的磷酸化
DOI：
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复制
发表时间：
2015
影响因子：
4.4
通讯作者：
Guo, Qulian
中科院分区：
文献类型：
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作者：
Ye, Zhi;Xia, Pingping;Cheng, Zhi-gang;Guo, Qulian
