The protective role of circ_0016760 downregulation against sevoflurane‑induced neurological impairment via modulating miR‑145 expression in aged rats

Sevoflurane can produce toxicity to the hippocampal tissues of brain, leading to nerve damage, causing learning and cognitive dysfunction. CircRNAs have been indicated to act as a key mediator in anesthetic neurotoxicity. This study focused on the effect of circ_0016760 on sevoflurane‑induced neurological impairment. The GEO database (GSE147277) and RT‑qPCR were used to predict and measure the circ_0016760 expression. The interaction of circ_0016760 and miR‑145 was verified by dual‑luciferase reporter assay. The CCK‑8 assay, flow cytometry, ELISA, ROS kit, MWM test were carried out to measure the cell viability, apoptosis, inflammation indicators, ROS level, and cognitive and memory function of the rats. Sevoflurane exacerbated neurotoxicity by restraining cell viability, inducing cell apoptosis, neuroinflammation, and ROS generation, and causing learning and cognitive dysfunction. Circ_0016760 expression was increased in POCD patients from the GEO database and upregulated after sevoflurane exposure. miR‑145 was a target miRNA of circ_0016760. Silencing of circ_0016760 weakened the effect of sevoflurane on cell viability, cell apoptosis, inflammation‑related factors, oxidative stress, which could be reversed by miR‑145 inhibitor. The animal experiments results showed that circ_0016760 played a protective effect on regulating the cognitive behavior of sevoflurane‑treated aged rats, expression of inflammation cytokine, and oxidative stress factors through targeting miR‑145 in sevoflurane‑treated aged rat’s hippocampal neurons. Our results revealed that silencing of circ_0016760 attenuated sevoflurane‑induced hippocampal neuron injury by regulating miR‑145 expression, which may provide potential insights into the treatment of sevoflurane‑induced neurological impairment.