Abstract:
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 hypoxia-injured 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/β-catenin and PI3K/AKT signaling pathways. And the activation of these two signaling induced by Sappanone A were repressed by miR-15a overexpression 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/β-catenin and PI3K/AKT signaling pathways.
journal_name
Int J Biol Macromoljournal_title
International journal of biological macromoleculesauthors
Kang C,Gao J,Kang M,Liu X,Fu Y,Wang Ldoi
10.1016/j.ijbiomac.2018.11.002subject
Has Abstractpub_date
2019-02-15 00:00:00pages
35-41eissn
0141-8130issn
1879-0003pii
S0141-8130(18)32954-4journal_volume
123pub_type
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