Objective To investigate the protective effect of dexmedetomidine(DEX)on sevoflurane induced learn-ing and cognitive impairment,and explore its potential mechanism.Methods Sprague-Dawley rat pups were exposed to 0.85％sevoflurane for a duration of 6 hours,followed by administration of varying doses of DEX.The Morris water maze test was employed to assess the cognitive and mnemonic capabilities of the rats.Western blot analysis was conducted to determine protein levels associated with the HIPK2/AKT/mTOR signaling pathway.TUNEL staining and flow cytometry techniques were utilized for apoptosis detection.Results The water maze results showed that sevoflurane treatment increased the escape latency of rats,but reduced the time in the original quadrant.DEX treatment dose-reversed the effects of sevoflurane on the latency and time of the original quadrant escape.DEX administration mitigated nerve damage and neuronal toxicity induced by sevoflurane.In addition,sevoflurane induced a significant increase in the protein levels of HIPK2,p-AKT,and p-mTOR,while DEX administration reduced the expression levels of these proteins.Administration of HIPK2 inhibitor A64 alleviated nerve damage and neuronal toxicity induced by sevoflurane.Conclusion DEX may protect the developing rat brain from se-voflurane-induced neurological dysfunction by regulating the HIPK2/AKT/mTOR signaling pathway.
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