Abstract: Abstract: Objective To investigate the protective effects of dexmedetomidine on bupivacaine-induced neurotoxicity. Methods Mouse neuroblastoma cell line N2a cells were divided into four groups. The cells in the control group were incu⁃ bated with no drug adding while the cells in bupivacaine group were treated with 1 000 µmol/L bupivacaine for 24 h. The cells in the group Dex1 and Dex2 were incubated with 1 000 µmol/L bupivacaine and 50 µmol/L, 200 µmol/L dexmedetomi⁃ dine for 24 h respectively. MTT assay was used to evaluate the cell viability. The reactive oxygen species (ROS) activity, mito⁃ chondrial membrane potential (MMP), the expression of Caspase-3 and apoptotic rate of N2a cells were detected by flow cy⁃ tometry. Results The cell viabilities were significantly decreased after being treated with 1 000 µmol/L bupivacaine, MMP was also significantly decreased, and apoptotic rates, levels of ROS and Caspase-3 were significantly increased. The bupiva⁃ caine-induced cytotoxicity was inhibited by dexmedetomidine (50 and 200 µmol/L), which resulted in the increase in the cell viability and MMP, but decrease in apoptotic rate and levels of ROS and Caspase-3. These effects were more significant in 200 µmol/L dexmedetomidine group than those of 50 µmol/L dexmedetomidine group. Conclusion Dexmedetomidine at⁃ tenuates bupivacaine-induced cytotoxicity of N2a cells, which may be related with the inhibition of ROS, the decrease in MMP and Caspase-3, and inhibiting appotosis in N2a cells.

Key words: dexmedetomidine, bupivacaine, apoptosis, reactive oxygen species, flow cytometry, neurotoxicity, mitochondrial membrane potential