LAUSR

Cerebral ischemia-reperfusion (I/R) injury is a terrible disease which results in the dysfunction and structural damage of brain tissues. Growing evidence implies that miR-455-5p is implicated in the regulation of pathogenesis of several diseases. The aim of this study is to reveal the role of miR-455-5p in cerebral I/R injury as well as the regulatory mechanism. We established a vitro model by inducing SH-SY5Y and PC-12 cells with oxygen-glucose deprivation and reoxygenation (OGD/R). The experimental cerebral I/R rat model was established by middle cerebral artery occlusion (MCAO) operation. The findings indicated that miR-455-5p expression was downregulated in OGD/R induced cells and I/R rat model. Additionally, miR-455-5p upregulation inhibited SH-SY5Y cell apoptosis and cerebral damage, while miR-455-5p silencing promoted SH-SY5Y cell apoptosis and cerebral damage. Mechanistically, luciferase reporter assay corroborated that miR-455-5p could bind with FMS-like tyrosine kinase 3 (FLT3) mRNA. However, the role of FLT3 in cerebral I/R injury was rarely investigated. RT-qPCR revealed that FTL3 expression was negatively regulated by miR-455-5p. FTL3 upregulation reversed the inhibitory effects of miR-455-5p upregulation on PC-12 and SH-SY5Y cell apoptosis. Therefore, our study verified that miR-455-5p improved cerebral I/R injury via targeting FLT3, which suggests a potential new target for the prevention of cerebral I/R injury.