Objective: We aimed to explore the effect of Sappanone A on neurologic damage induced by hypoxia.
Methods: PC-12 cells were pre-treated with Sappanone A and were simulated by hypoxia. miRNA transfection was performed to overexpress or suppress the expression of miR-15a in PC-12 cells. Cell viability, apoptosis, migration, and expression levels of miR-15a were tested to evaluate the in vitro impact of Sappanone A on hypoxiainjured PC-12 cells.
Results: Hypoxia exposure induced a significant damage in PC-12 cells, as evidenced by the repressed cell growth, the induced apoptosis and the impaired migrating capacity. Sappanone A pretreatment protected PC-12 cells against hypoxia-mediated cell damage. More interestingly, Sappanone A treatment down-regulated miR-15a, and the neuroprotective effects of Sappanone A were attenuated by miR-15a overexpression while were accelerated by miR-15a suppression. Finally, Sappanone A significantly activated Wnt/beta-catenin and PI3K/AKT signaling pathways. And the activation of these two signaling induced by Sappanone A were repressed by miR-15a over expression and were enhanced by miR-15a suppression.
Conclusion: Sappanone A exerted protective activity in PC-12 cells which were stimulated by hypoxia. One of the possible mechanisms of the neuroprotective effect is that: Sappanone A down-regulated the expression of miR-15a, and thus activated Wnt/beta-catenin and PI3M/AKT signaling pathways. (C) 2018 Published by Elsevier B.V.