Abstract
In the present study, the mechanisms underlying the protective effects of microRNA‑132 (miRNA‑132) on sevoflurane‑induced neuronal apoptosis were investigated. Reverse transcription‑quantitative polymerase chain reaction and gene microarray hybridization were used to analyze alterations in microRNA levels. Cell viability, apoptosis and caspase‑3/9 activity were measured using MTT, flow cytometry and caspase‑3/9 activity kits. Immunofluorescence staining and western blot analysis were used to measure protein expression of phosphoinositide 3‑kinase (PI3K) and phosphorylated (p‑)AKT, forkhead box O3a (FOXO3a). In sevoflurane‑induced rats, the expression of miRNA‑132 was downregulated, compared with that in negative control rats. The downregulation of miRNA‑132 increased neuronal apoptosis and the upregulation of miRNA‑132 inhibited neuronal apoptosis in the sevoflurane‑induced in vitro model. The downregulation of miRNA‑132 suppressed the protein expression of PI3K and p‑AKT, and suppressed the protein expression of FOXO3a in the sevoflurane‑induced in vitro model. The PI3K inhibitor increased the effects of anti‑miRNA‑132 on neuronal apoptosis through the AKT/FOXO3a pathway in the sevoflurane‑induced in vitro model. The promotion of FOXO3a inhibited the effects of anti‑miRNA‑132 on neuronal apoptosis through the AKT/FOXO3a pathway in the sevoflurane‑induced in vitro model. These data suggested that miRNA‑132 caused sevoflurane‑induced neuronal apoptosis via suppression of the PI3K/AKT/FOXO3a pathway.