Isoflurane (ISO) is an anesthesia and can result in neuron injury. A previous study has indicated that microRNA-302b-3p (miR-302b-3p) exerts a crucial function in modulating cerebral ischemia/reperfusion damage-induced neuronal injury. We sought to examine the role of miR-302b-3p in ISO-induced neuronal injury. In the present study, the effects of miR-302b-3p on ISO-induced neuron injury were investigated by MTT and TUNEL assays. We discovered that ISO stimulation led to miR-302b-3p upregulation and neuronal injury. MiR-302b-3p silencing exerted protective effects against ISO induced neuronal injury. In addition, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) was a direct downstream target gene of miR-302b-3p. MiR-302b-3p targets the 3'UTR of PTEN to inhibit its mRNA expression, and further reduces its protein expression. Silencing of PTEN partially reversed the protecting effects of silenced miR-302b-3p on ISO-induced injury of hippocampal neurons. Further, miR-302b-3p activated the AKT signaling pathway in neurons exposed to ISO by downregulation of PTEN. Finally, in vivo studies revealed that silencing of miR-302b-3p alleviates ISO-induced injury and spatial memory impairment of rats partly by upregulation of PTEN. Overall, our findings indicated that miR-302b-3p targets PTEN to activate the AKT pathway, and silencing of miR-302b-3p plays a neuroprotective role in ISO-induced neuronal injury by the PTEN/AKT pathway, suggesting miR-302b-3p as a crucial target for ISO-induced neuronal injury.
Keywords: AKT; Isoflurane; Neuroprotection; PTEN; miR-302b-3p.
Copyright © 2020. Published by Elsevier Inc.