RESUMO
MicroRNAs (miRs) have been proposed to be involved in the pathological processes of cerebral ischemia/reperfusion (CIR) injury. The present study aimed to investigate the potential role and molecular mechanisms of miR217 in the regulation of neuronal survival in CIR injury. To perform the investigation, an in vitro cellular model of CIR injury was established by treating neurons with oxygenglucose deprivation and reoxygenation (OGD/R). miR217 levels in neurons were detected using reverse transcriptionquantitative PCR. The association between miR217 and sirtuin 1 (SIRT1) was identified using TargetScan and validated in a dualluciferase reporter assay. Cell viability and apoptosis were measured using a Cell Counting Kit8 assay and flow cytometry, respectively. The release of lactate dehydrogenase, and the production of proinflammatory factors and oxidative stress biomarkers were analyzed by ELISAs and using specific assay kits. It was revealed that miR217 was significantly upregulated in OGD/Rtreated neurons. SIRT1 was a direct target of miR217, and was downregulated in neurons following OGD/R treatment. Downregulation of miR217 significantly ameliorated OGD/Rinduced neuronal injury, inflammatory responses and oxidative stress. The effects of miR217 inhibitor on OGD/R treated neurons were attenuated by SIRT1 knockdown. Additionally, western blotting revealed that the SIRT1/AMPactivated protein kinaseα/NFκB pathway was partially involved in the regulation of OGD/Rinduced neuronal injury by miR217. In conclusion, the data of the present study indicated that the downregulation of miR217 protected neurons against OGD/Rinduced injury by targeting SIRT1.