miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP
- Yihan Wang
- Jiahui Jin
- Zongxin Xia
- Huisheng Chen
Affiliations: Department of Neurology, General Hospital of Northern Theater Command, Shenyang, Liaoning 110013, P.R. China, Department of Neurology, Jilin City Central Hospital, Jilin, Jilin 132011, P.R. China, Department of Neurology, Baishan City Central Hospital, Baishan, Jilin 134399, P.R. China
- Published online on: August 31, 2022 https://doi.org/10.3892/mmr.2022.12838
Copyright: © Wang
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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.