换一批
换一批Activation of Akt/FoxO and inactivation of MEK/ERK pathways contribute to induction of neuroprotection against transient global cerebral ischemia by delayed hypoxic postconditioning in adult rats.
第一作者：
Lixuan,Zhan
第一单位：
Institute of Neurosciences and the Second Affiliated Hospital of Guangzhou Medical College, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, 250 Changgang Dong RD, Guangzhou 510260, China.
作者：
主题词
动物(Animals);CA1区, 海马(CA1 Region, Hippocampal);细胞死亡(Cell Death);脑血管循环(Cerebrovascular Circulation);减量调节(Down-Regulation);酶激活(Enzyme Activation);酶抑制剂(Enzyme Inhibitors);叉头转录因子类(Forkhead Transcription Factors);脑缺血发作, 短暂性(Ischemic Attack, Transient);缺血后处理(Ischemic Postconditioning);MAP激酶信号系统(MAP Kinase Signaling System);男(雄)性(Male);神经组织蛋白质类(Nerve Tissue Proteins);神经元(Neurons);磷酸肌醇3-激酶类(Phosphatidylinositol 3-Kinases);磷酰化(Phosphorylation);蛋白质加工, 转译后(Protein Processing, Post-Translational);原癌基因蛋白质c-akt(Proto-Oncogene Proteins c-akt);随机分配(Random Allocation);大鼠(Rats);大鼠, Wistar(Rats, Wistar);时间因素(Time Factors)
DOI
10.1016/j.neuropharm.2012.06.035
PMID
22749925
发布时间
2022-03-21
- 浏览142
Neuropharmacology
873-82页
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