Up-regulation of miR-490-3p improves learning/memory disability of sevoflurane exposure by relieving neuroinflammation

Our study focused on the potential mechanism of microRNA-490-3p (miR-490-3p) on learning/memory disability of rats resulting from sevoflurane (Sev). The rat model of cognitive dysfunction was established by infection with miR-490-3p mimic and Sev-exposure. Morris water maze and open field test assay were used for the assessment of cognitive deficits. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction assays were used for the measurements of neuroinflammatory cytokines and inflammatory-related genes in respective order. Bioinformatics analysis was employed for the predictive miR-490-3p-related genes. The targeted interaction was verified via dual-luciferase reporter assay. A significant decline of miR-490-3p was discovered in rats with Sev treatment, while the levels were up-regulated in rats with infection miR-490-3p pretreatment (<i>P</i> < 0.001). For Sev-induced rats, the stay time in the target quadrant was shorten, while distance travelled lengthened significantly with the control group by comparison (<i>P</i> < 0.001). Notably, an increased time of the escape latency and a decreased number of platform crossings were found in the Sev group, which alleviated by infection with miR-490-3p mimic pretreatment (<i>P</i> < 0.001). Moreover, the neuroinflammatory cytokines were elevated in the Sev group, the effects of which were recovered via miR-490-3p pretreatment (<i>P</i> < 0.001). Bioinformatics analysis predicted the miR-490-3p-associated genes. CDK1 (Cyclin-dependent kinase 1) was a potential target gene of miR-490-3p, which confirmed by dual-luciferase reporter detection. MiR-490-3p alleviated the learning and memory deficits in Sev-treated rats via the modulation of CDK1.