miR-363-3p attenuates the oxygen-glucose deprivation/reoxygenation-induced neuronal injury in vitro by targeting PDCD6IP

The purpose of the present study was to explore the functional role of microRNA (miR)-363-3p and related regulatory mechanisms in cerebral ischemia/reperfusion (I/R) injury. The neuronal cell line SH-SY5Y was exposed to 4 h of oxygen and glucose deprivation (OGD), followed by 6, 12, 24 and 48 h of re-oxygenation to mimic I/R injury in vitro. Cell viability, apoptosis and inflammation were assessed by CCK-8, lactate dehydrogenase (LDH), flow cytometry and ELISA assays. The association between miR-363-3p and programmed cell death 6-interacting protein (PDCD6IP) was further confirmed using luciferase reporter assay. Our data revealed that the expression level of miR-363-3p was significantly downregulated after OGD/R induction. Overexpression of miR-363-3p markedly suppressed OGD/R-induced cell injury, as reflected by attenuated cell viability, reduced apoptosis, LDH activity and pro-inflammatory cytokine levels. Mechanistically, PDCD6IP was confirmed as the target of miR-363-3p. Furthermore, PDCD6IP knockdown imitated, while overexpression reversed the effects of miR-363-3p overexpression on OGD/R-induced cell injury. Collectively, miR-363-3p could attenuate OGD/R-induced cell injury by alleviating apoptosis and inflammation, which may be mediated, at least in part, via inhibition of PDCD6IP.