Abstract: Objective: Investigate the important effects of 14-3-3 phosphorylation induced by JNK on ischemic brain injury in rats. Methods: Reproduced the four-vessel occlusion model of cerebral ischemia in rats. 14-3-3 phosphorylation, the binding of 14-3-3 and Bad, protein expression of Bax in cytoplasm and mitochondria in hippocampal CA1 region were detected by immunoprecipitation (IP) and immunoblotting (IB) 12 hour after ischemia reperfusion. Results: Compared with the sham operation group, SP600125, an inhibitor of JNK, inhibited 14-3-3 phosphorylation, promoted the binding of 14-3-3 and Bad, lessened the expression of Bax in mitochondria in hippocampal CA1 region. Conclusion: 14-3-3 phosphorylation induced by JNK played important effects on ischemic brain injury in rats, which provided a new idea for clinical control of human ischemic stroke.

Key words: 14-3-3 phosphorylation, JNK, Bax, Cerebral ischemia