Objective: To analyze the inhibition of sevoflurane-induced neuronal apoptosis by dexmedetomidine via activating the mitogen-active protein kinase-cAMP response element-binding protein-brain-derived neurotrophic factor (MAPK-CREB-BDNF) signaling pathway.Methods: Seventy-two healthy male SD rats of clean grade were randomly selected, and the rats were randomly divided into a control group, model group, and a dexmedetomidine group, with 24 rats in each group. Rats in the model group and the dexmedetomidine group had sevoflurane concentration of about 0.75% for six hours. Rats in the dexmedetomidine group were intraperitoneally injected with dexmedetomidine for 10 h, and rats in the control group were fed normally. A Morris water maze was used to determine the escape latency, the original platform quadrant residence time and the number of times crossing the platform. The TUNEL method was used to determine neuronal apoptosis in each group. A protein imprinting method was used to determine the apoptosis-related protein Caspase-3, Bcl-2, Bax, ERK1/2, CREB, and BDNF in each group of rats.Results: There was no significant difference in the first day of escape latency between the three groups (P>0.05). From the second day, the escape latency increased significantly in the model group compared with the control group, and the residence time of the original platform quadrant and the times of crossing the platform decreased significantly (P>0.05). Compared with the model group, the escape latency of the dexmedetomidine group was significantly reduced, while the residence time and times of crossing the platform in the original platform quadrant were significantly increased (P<0.05). Compared with the control group, the expression levels of Caspase-3 and Bax in the model group were significantly increased, while the expression levels of Bcl-2, ERK1/2, CREB and BDNF were significantly decreased (P<0.05). Compared with the model group, the expression levels of apoptosis, Caspase-3 and Bax in the dexmedetomidine group were significantly reduced, and the expression levels of Bcl-2, ERK1/2, CREB and BDNF were significantly increased (P<0.05).Conclusion: Dexmedetomidine can significantly inhibit sevoflurane-induced neuronal apoptosis and cognitive dysfunction by activating the MAPK-CREB-BDNF signaling pathway.
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