Conclusion
Our findings revealed the role and mechanism of miRNA-384-3p in sevoflurane-induced nerve injury, suggesting that miRNA-384-3p could be a novel and promising strategy for reducing sevoflurane-induced neurotoxicity.
Methods
Seven-day-old rats were exposed to 2.3% sevoflurane to induce nerve injury. The morphological changes in neurons in the hippocampal CA1 region were detected by HE staining and Nissl staining. Neuronal apoptosis was detected by TUNEL and Western blot assays. Spatial memory and learning ability were detected by the Morris water maze assay. The target gene of miRNA-384-3p was verified through a luciferase reporter assay. A rescue experiment was used to confirm the miRNA-384-3p pathway in sevoflurane-induced nerve injury.
Objective
Sevoflurane is a common anesthetic and is widely used in pediatric clinical surgery to induce and maintain anesthesia through inhalation. Increasing studies have revealed that sevoflurane has neurotoxic effects on neurons, apoptosis, and memory impairment. miR-384 is involved in the process of neurological diseases. However, the role of miRNA-384-3p in sevoflurane-induced nerve injury is not clear. This study focused on exploring the roles and mechanisms of miRNA-384-3p in sevoflurane-induced nerve injury.
Results
Sevoflurane reduced miRNA-384-3p expression in the rat hippocampus. miRNA-384-3p alleviated sevoflurane-induced morphological changes in hippocampal neurons and apoptosis of neurons in the hippocampal CA1 region. Meanwhile, miRNA-384-3p attenuated the decline in spatial memory and learning ability induced by sevoflurane. miRNA-384-3p alleviated sevoflurane-induced nerve injury by inhibiting the expression of adaptor-associated kinase 1 (Aak1).