钙调素依赖性蛋白激酶Ⅱ在盐酸布比卡因诱导SH-SY5Y细胞损伤中的作用

目的探讨钙调素依赖性蛋白激酶Ⅱ（CaMKⅡ）抑制剂KN93对盐酸布比卡因诱导的人神经母细胞瘤细胞（SH-SY5Y细
胞）损伤的影响。方法SH-SY5Y细胞随机分为4组（n=6）：正常培养组（C组）；KN93组（K组，KN93终浓度1 μmol/L孵育24 h）；
布比卡因组（B组，盐酸布比卡因终浓度1 mmol/L孵育24 h）；KN93+布比卡因组（KB组，KN93终浓度1 μmol/L和盐酸布比卡
因终浓度1 mmol/L孵育24 h）。孵育24 h后在显微镜下观察各组细胞形态改变及免疫印迹法检测各组细胞Cav3.1亚型T型钙
通道（Cav3.1）蛋白的表达；在孵育前（T1）、孵育后1 h（T2）、6 h（T3）、12 h（T4）、24 h（T5）MTT法检测细胞活力及流式细胞仪检测细
胞凋亡率。结果SH-SY5Y细胞经1 mmol/L盐酸布比卡因处理后，细胞突触消失，胞体变圆；细胞活力降低；细胞凋亡率升高；
Cav3.1蛋白的表达上调；1 mmol/L的KN93则可以减少盐酸布比卡因所致的上述改变的幅度。结论CaMKⅡ可能参与盐酸布
比卡因所致的SH-SY5Y细胞损伤，且与上调Cav3.1蛋白的表达有关。

Role of calmodulin-dependent protein kinase II in bupivacaine hydrochloride-induced injury of SH-SY5Y cells

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.