Abstract
Sevoflurane (Sev) is a widely applied anesthetic in clinical practice; however, it could induce neurotoxicity and lead to postoperative cognitive dysfunction (POCD). This study aimed to investigate the role and underlying mechanism of circHOMER1 in Sev-induced neurotoxicity and POCD. Sev treated mouse hippocampal neuronal HT22 cells and SD rats. RT-qPCR was used to detect the levels of circHOMER1 and miR-217. ELISA was employed to measure the levels of inflammatory factors IL-6, IL-1β, and TNF-α. Commercially available kits assessed the concentration of MDA and measured the activities LDH and SOD. The CCK-8 assay assessed cell viability. Flow cytometry analyzed cell apoptosis. The Morris water maze test evaluated the learning and cognitive abilities of the rats. Dual luciferase reporter assays and RIP experiments validated the targeted binding of circHOMER1 to miR-217. Sev treatment significantly reduces cell viability, increases apoptosis, stimulates inflammatory responses and oxidative stress, and induces learning and memory impairments in SD rats. Following exposure to Sev, the expression of circHOMER1 is markedly decreased, while overexpression of circHOMER1 can alleviate Sev-induced neuroinflammation, oxidative stress, and learning and memory deficits in rats. CircHOMER1 targets miR-217, and transfection of miR-217 antagonizes the neuroprotective effects of circHOMER1. This study demonstrated that circHOMER1 negatively regulated miR-217, thereby inhibiting Sev-induced neurotoxicity and learning and memory disorders.
Published Version
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