KIF 2 mediates the neuroprotection in cerebral ischaemia injury by affecting NF ‐κB pathway

Stroke is the most common cerebrovascular disease with high morbidity and mortality around the world. However, the underlying mechanisms involved in nerve injury and cerebral ischaemia/reperfusion (I/R) during cerebrovascular disease are still not completely clear. In the present study, we investigate the role of kinesin family member 2 ( KIF 2) in the neuroprotection after cerebral I/R injury. KIF 2 was aberrantly expressed in the cerebral tissues from middle cerebral artery occlusion ( MCAO ) rat model in a time dependent manner. A similar changing pattern was found in the cultured hypoxic neurons as well as SK ‐N‐ SH cells in vitro. Compared to the control, KIF 2 inhibition significantly increased the level of malonic dialdehyde ( MDA ), and reduced the level of superoxide dismutase ( SOD ) as well as glutathione peroxidase (GSH‐px) activity in cerebral tissues of MCAO rat model. The reactive oxygen species ( ROS ) level was also up‐regulated after KIF 2 si RNA knockdown in cultured hypoxic SK ‐N‐ SH cells. The apoptosis rates of hypoxic neurons and SK ‐N‐ SH cells as well as activated‐caspase‐3 level were obviously increased after KIF 2 silencing. Furthermore, we found that the nuclear factor‐kappa B ( NF ‐κB) pathway was involved in KIF 2‐mediated neuroprotection after cerebral I/R injury, and induced apoptosis of hypoxic SK ‐N‐ SH cells by KIF 2 silencing could be attenuated by the specific inhibitor BAY 11‐7082 of NF ‐κB. In conclusion, we demonstrate that KIF 2 could mediate the neuroprotection in cerebral I/R injury by inhibiting activation of NF ‐κB pathway. This might provide a novel therapeutic target for cerebral I/R injury.