医学
缺血
NADPH氧化酶
再灌注损伤
药理学
心脏病学
氧化应激
内科学
作者
Jia Zhou,Yihua Zhang,Huizhu Song,Hui Ji,Xiaoli Wang,Lei Wang,Jun Qian,Jingjing Ling,Fengfeng Ping
出处
期刊:Oncotarget
[Impact Journals, LLC]
日期:2016-05-12
卷期号:7 (26): 39444-39457
被引量:10
标识
DOI:10.18632/oncotarget.8548
摘要
5d, a novel analogue of the racemic 3-n-butylphthalide (NBP), has been reported for its free radical scavenging activity in vitro and preventive neuroprotection in vivo. Nevertheless, the mechanism by which 5d attenuated ischemia/reperfusion (I/R) injury is still unknown. Our results showed that 5d significantly increased CK2 activity as well as CK2α and 2α' protein levels after I/R injury. Besides, 5d suppressed the translocation of cytosolic p47phox and Rac1 to the membrane, decreased NOX4 expression and ROS generation. Furthermore, 5d blocked the dissociation between CK2α and Rac1 so as to decrease NADPH oxidase activity. Based on these findings, we propose that the neuroprotective effect of 5d is due to an increase of CK2 activity, which blocks I/R-induced dissociation between CK2α and Rac1, decreases NADPH oxidase activity, inhibits ROS production and finally realizes the neuroprotection of I/R. These findings point to that 5d might be considered an attractive candidate for further studies in ischemic stroke.
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