miR-30b protects microglia deprived with oxygen and glucose via regulating inflammatory response
Abstract：Ischemic stroke is considered to be the leading cause of mortality and morbidity through the world. In the present study, we evaluated the role of miR-30b and its direct target, mixed lineage kinase 4 (MLK4), in ischemic stroke in an in vitro model. Murine microglia BV-2 cells were cultured with oxygen-glucose deprivation (OGD). Expression changes of miR-30b and MLK4 were detected. BV-2 cells were then transfected with miR-30b mimic. The impact of miR-30b expression level on cellular apoptosis, expression of MLK4, and expression of inflammatory factors were measures. Dual-luciferase reporter assay was performed to test the direct targeting relation between miR-30b and MLK4. OGD treatment significantly down-regulated the level of miR-30b, while up-regulated both the protein and mRNA levels of MLK4 in a time-dependent manner. The expression of MLK4 was negatively regulated by miR-30b by a direct interaction. The addition of miR-30b mimic significantly inhibited the apoptosis induced by OGD treatment. Moreover, the increased levels of inflammatory cytokines, such as IL-1β, IL-6 and TNF-α, under OGD condition, were also decreased by miR-30b mimic. In conclusion, miR-30b protects microglia via inhibiting the apoptosis and inflammation under OGD condition. Therefore miR-30b might be a new therapeutic target for ischemic stroke.