Overexpression of miR‐224‐3p alleviates apoptosis from cerebral ischemia reperfusion injury by targeting FIP200

Abstract Aims In previous studies, numerous differential microRNAs (miRNAs) in cerebral ischemic/reperfusion (I/R) injury were identified using the miRNA microarray analysis. However, the relationship between miRNA and cerebral I/R injury remains largely unknown. In this study, we investigated the function and explored the possible mechanism of miR‐224‐3p in cerebral I/R injury. Methods Oxygen glucose deprivation model in N2a cells were used to perform the cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase‐3 were measured to evaluate the function of miR‐224‐3p. Results Overexpression of miR‐224‐3p alleviated the apoptosis induced by oxygen glucose deprivation (OGD) and cleaved caspase‐3 was significantly reduced. We further provided the possible mechanism that miR‐224‐3p may protect cells from cerebral I/R injury by targeting FAK family‐interacting protein (FIP200). Further rescue experiment proved that overexpression of FIP200 partially blocked the effect of miR‐224‐3p. Conclusions We evaluated the function and mechanism of miR‐224‐3p in ischemic brain injury. miR‐224‐3p may serve as a potential target for new therapeutic intervention.