Knockdown lncRNA Neat1 regulates the activation of microglia and alleviate neuronal apoptosis through AKT/STAT3 pathway after cerebral ischemic reperfusion.

Abstract Background Acute cerebral ischemia may cause serious consequences, one of them is brain injury caused by the uncontrolled reperfusion which occurs once the circulation is re-established. Neat1 is one of long non-coding RNA presents important roles in the immune system. However, the potential roles and underlying molecular mechanisms of it in cerebral ischemic reperfusion injury is still unclear.The aim of the present study was to investigate the function of LncRNA Neat1 in cerebral ischemic reperfusion injury and its possible advantage for neure.MethodsIn our study, oxygen glucose deprivation was used in vitro to mimic cerebral I/R injury. CCK8 was used to mesure cell viability and flow cytometry measured cell apoptosis. qRT-pcr was used to measure the phenotypic marker of M1 and M2 microglia, western blot was used to detect the protein expression of AKT/STAT3 pathway.ResultsKnockdown the LncRNA Neat1 alleviated the apoptosis induced by OGD/R and increased the cell viability.We further provided that Neat1 may inhibite microglia polarize to M1 phenotype to reduce the damage of immunoreaction caused after cerebral I/R injury through AKT/STAT3 pathway. ConclusionsWe evaluated the function and mechanism of lncRNA Neat1 in cerebral I/R injury, And LncRNA Neat1 may be a potential target for new therapeutic intervention.