Polyamine analogue QMA attenuated ischemic injury in MCAO rats via ERK and Akt activated Nrf2/HO-1 signaling pathway

被引：22
作者：
Cen, Juan [1 ]
Zhao, Na [2 ]
Huang, Wei-wei [1 ]
Liu, Lu [3 ]
Xie, Yuan-yuan [1 ]
Gan, Ying [1 ]
Wang, Chao-jie [1 ]
Ji, Bian-Sheng [1 ]
机构：
[1] Henan Univ, Key Lab Nat Med & Immune Engn, Kaifeng 475001, Peoples R China
[2] Henan Med Coll, Dept Pharmacol, Zhengzhou 450000, Henan, Peoples R China
[3] Henan Univ, Sch Pharm, Kaifeng 475001, Peoples R China
来源：
EUROPEAN JOURNAL OF PHARMACOLOGY | 2019年 / 844卷
基金：
中国国家自然科学基金;
关键词：
QMA; Cerebral ischemia; Nrf2; HO-1; Reactive oxygen species; HEME OXYGENASE-1; OXIDATIVE STRESS; POTENTIAL ROLES; PC12; CELLS; APOPTOSIS; BRAIN; NRF2; EXPRESSION; FACTOR-2; PROTECTS;
D O I：
10.1016/j.ejphar.2018.12.015
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Previous research showed N-1-(quinolin-2-ylmethy) butane-1, 4-diamine (QMA), a polyamine analogue, was efficacious in the prevention of oxidative injury in models of cerebral ischemia. The present study manifested that pretreatment with QMA attenuated ischemic damage accompanying up regulation of Nuclear factor erythroid 2-related factor (Nrf2), Heme oxygenase-1 (HO-1), p-ERK and p-Akt in cerebral cortex tissues of middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation (OGD)-treated PC12 cells. Further more, treatment with LY294002 (specific PI3K inhibitor), PD98059 (specific ERK inhibitor), brusatol (specific Nrf2 inhibitor) and SnPP (specific HO-1 inhibitor) deprived almost all the effects of QMA in MCAO rats and OGD-treated PC12 cells. These data suggested that the protective actions of QMA on the cerebral ischemia may be related to activation of endogenous cytoprotective mechanism via ERK and Akt activated Nrf2/HO-1 signaling pathway.
引用
收藏
页码：165 / 174
页数：10
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