LAUSR

BACKGROUND Sevoflurane (Sevo) is neuroprotective in brain damage, thus our objective was to further investigate the impact of Sevo treatment on nerve regeneration and repair of neurological deficit in brain damage rats by regulating miR-490-5p and cyclin-dependent kinases 1 (CDK1). METHODS The rat middle cerebral artery occlusion model was established. miR-490-5p and CDK1 levels in brain tissues were tested. The behavioral changes, the number of glial fibrillary acidic protein (GFAP) positive cells, ionized calcium-binding adapter molecule-1 (Iba-1) and Nestin mRNA expression, the survival and apoptosis of neurons in peripheral tissues of infarct areas were detected by a series of assays. Furthermore, the target relationship between miR-490-5p and CDK1 was verified. RESULTS miR-490-5p was reduced and CDK1 was raised in brain tissues of brain damage rats. Sevo raised miR-490-5p and decreased CDK1 to improve neurological deficits, reduce apoptotic neurons, suppress expression levels of GFAP and Iba-1, and increase Nestin expression and the number of surviving neurons in peripheral tissue in infarct area, and alleviate the pathological changes of brain tissues of brain damage rats. CDK1 was negatively regulated by miR-490-5p. CONCLUSION Our study presents that Sevo treatment is involved in neurogenesis and repair of neurological deficit of brain damage rats via up-regulating miR-490-5p and inhibiting CDK1.