Kalirin-7 plays the neuroprotective role in Neuro-2A cells injured by oxygen-glucose deprivation and reperfusion through Rac1 activation

Document Type: Original Article


1 Department of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao 266500, China

2 Department of Neurology, Liaocheng People’s Hospital, Liaocheng 252000, China


Objective(s): The study explored the neuroprotective role of Kalirin-7 (Kal-7) in Neuro-2A cells after oxygen-glucose deprivation and reperfusion (OGD/R) treatment.
Materials and Methods: The study used an OGD/R model of mouse Neuro-2A neuroblastoma cells in vitro. Cells were transfected with pCAGGS-Kal-7 to up-regulating kal-7. Then cell proliferation and apoptosis were respectively analyzed by Trypan blue exclusion method and flow cytometry. To examine the involvement of Rac1, cells were treated with Rac1-GTP inhibitor NSC23766 before treatment with OGD/R. Expressions of Bax, Bcl-2, Rac1, and down-stream targets of Rac1 were analyzed by Western blot.
Results: Kal-7 significantly decreased OGD/R induced cell apoptosis (P<0.01), but no significant effects were observed on cell proliferation. Kal-7 increased the expressions of apoptosis-related protein of Bcl-2 and Rac1, but decreased the expression of Bax in Neuro-2A cells stimulated to OGD/R. Rac1 was activated by Kal-7 due to the increased levels of its down-stream targets, p-p38 and p-PAK1. NSC23766 reduced the anti-apoptotic effect of Kal-7 as the enhanced apoptotic cell rate and increased Bax/Bcl-2 ratio.
Conclusion: These findings suggest that the protective effects of Kal-7 against OGD/R injury in Neuro-2A cells were dependent in a Rac1 activation signaling.


Main Subjects

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