Retracted : Upregulated microRNA‐31 inhibits oxidative stress‐induced neuronal injury through the JAK/STAT3 pathway by binding to PKD1 in mice with ischemic stroke

Ischemic stroke (IS), which is characterized by high morbidity, disability, and mortality, is recognized as a major cerebrovascular disease. MicroRNA‐31 (miR‐31) was reported to participate in the progression of brain disease. The present study was conducted in order to investigate the effect of miR‐31 on oxidative stress‐induced neuronal injury in IS mice with the involvement of protein kinase D1 (PKD1) and the JAK/STAT3 pathway. C57BL/6J mice were used to establish the middle cerebral artery occlusion (MCAO) model. Astrocytes were transfected with miR‐31 mimic, miR‐31 inhibitor, si‐PKD1, or JAK‐STAT3 pathway inhibitor. Following the establishment of an oxygen–glucose deprivation (OGD) model, the astrocytes were cocultured with neuronal OGD. Lower miR‐31, higher PKD1 expressions, and activated JAK/STAT3 pathway were found in both the MCAO and OGD models. miR‐31 could negatively target PKD1. In an MCAO model, overexpressing miR‐31 and silencing PKD1 reduced neuronal injury, cerebral infarct volume, neuron loss, and oxidative stress injury, inhibited the activation of JAK/STAT3 pathway and the expressions of PKD1, interleukin (IL)‐1β, IL‐6, tumor necrosis factor‐α, malondialdehyde, 4‐HNE, 8‐HOdG, caspase‐3, and Bax, but increased the superoxide dismutase content. In the OGD model, overexpression of miR‐31 and silencing of PKD1 attenuated oxidative stress‐induced neuronal injury, and diminished the lactate dehydrogenase leakage and reactive oxygen species level, accompanied by elevated neuronal viability. These results indicate that miR‐31 alleviates inflammatory response as well as an oxidative stress‐induced neuronal injury in IS mice by downregulating PKD1 and JAK/STAT3 pathway.