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Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3β through the PI3K/Akt survival pathway
Ye, Zhi; Xia, Pingping; Cheng, Zhi-gang; Guo, Qulian*
刊名Journal of the Neurological Sciences
2015
卷号348期号:1-2页码:216-225
关键词Apoptosis Focal cerebral ischemia Glycogen synthase kinase 3beta (GSK-3beta) PI3K/Akt Post-conditioning Sevoflurane
ISSN号0022-510X
DOI10.1016/j.jns.2014.12.011
URL标识查看原文
WOS记录号WOS:000349588300033
内容类型期刊论文
URI标识http://www.corc.org.cn/handle/1471x/3333478
专题中南大学
作者单位1.[Guo, Qulian
2.Xia, Pingping
3.Cheng, Zhi-gang
4.Ye, Zhi] Affiliated Xiangya Hosp Cent South Univ, Dept Anesthesiol, Changsha 410078, Hunan, Peoples R China.
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GB/T 7714
Ye, Zhi,Xia, Pingping,Cheng, Zhi-gang,et al. Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3β through the PI3K/Akt survival pathway[J]. Journal of the Neurological Sciences,2015,348(1-2):216-225.
APA Ye, Zhi,Xia, Pingping,Cheng, Zhi-gang,&Guo, Qulian*.(2015).Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3β through the PI3K/Akt survival pathway.Journal of the Neurological Sciences,348(1-2),216-225.
MLA Ye, Zhi,et al."Neuroprotection induced by sevoflurane-delayed post-conditioning is attributable to increased phosphorylation of mitochondrial GSK-3β through the PI3K/Akt survival pathway".Journal of the Neurological Sciences 348.1-2(2015):216-225.
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