Abstract
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.
Highlights
Strokes are the leading cause of permanent disability and death worldwide
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 reactive oxygen species (ROS) production and realizes the neuroprotection of I/R
The middle cerebral artery occlusion (MCAO) was used as an in vivo model, while the oxygen-glucose deprivation/reoxygen (OGD/R) was used as an in vitro model. The aim of this text is to investigate whether CK2 and/or NADPH oxidase are involved in neuroprotection of 5d against the cerebral ischemia and its relevant mechanism
Summary
Strokes are the leading cause of permanent disability and death worldwide. Due to the occlusion of a vessel in the brain, ischemic strokes account for the majority of strokes [1, 2]. To improve its therapeutic effect, NBP is often administered with anti-platelet and/or antioxidant drug(s) [8] It has been recently reported the actions of 5d against free radicals, platelet aggregation, thrombosis and cerebral ischemia [9]. The middle cerebral artery occlusion (MCAO) was used as an in vivo model, while the oxygen-glucose deprivation/reoxygen (OGD/R) was used as an in vitro model. The aim of this text is to investigate whether CK2 and/or NADPH oxidase are involved in neuroprotection of 5d against the cerebral ischemia and its relevant mechanism
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