Abstract: Objective To investigate the effect of KN93, a calmodulin-dependent protein kinase II (CaMK II) inhibitor, on
SH-SY5Y cell injury induced by bupivacaine hydrochloride. Methods SH-SY5Y cells exposed for 24 h to 1 mmol/L KN93, 1
mmol/L bupivacaine hydrochloride, or both were examined for morphological changes and Cav3.1 protein expressions using
Western blotting. The vitality and apoptosis rate of the cells at different time points during the exposures were assessed with
MTT assay and flow cytometry, respectively. Results Bupivacaine hydrochloride exposure caused obvious cell morphologial
changes, reduced cell viability, increased cell apoptosis, and enhanced Cav3.1 protein expression. All these changes were
partly reversed by treatment of the cells with 1 mmol/L KN93. Conclusion CaMKII may play a role in bupivacaine
hydrochloride-induced SH-SY5Y cells injury, which is related with upregulated Cav3.1 protein expression.