中文摘要：

目的评价钙／钙调素依赖性蛋白激酶Ⅱ（CaMKⅡ）在利多卡因诱发神经细胞损伤中的作用。方法培养SH—SY5Y细胞，以5×10^5个／ml的密度接种于96孔（100μl／孔）培养板。采用随机数字表法，将细胞随机分为4组（n=63）：常规培养组（C组）；CaMKlI抑制剂KN93组（K组）在细胞培养液中加入KN93（终浓度1μmol／L）孵育24h；利多卡因组（L组）在细胞培养液中加入利多卡因（终浓度10mmol／L）孵育24h；KN93＋利多卡因组（KL组）在细胞培养液中加入KN93（终浓度1μmol／L）和利多卡因（终浓度10mmol／L）孵育24h。药物孵育24h后，镜下观察细胞病理学结果。于药物孵育前、孵育l、6、12、24h时采用MTT法检测细胞活力及流式细胞仪检测细胞凋亡情况。结果与C组和K组比较，L组和KL组细胞活力降低，细胞凋亡率升高（P〈O．05）。与L组比较，KL组细胞活力升高，细胞凋亡率降低（P〈0．05）。C组和K组各指标比较差异无统计学意义（P〉0．05）。L组细胞病理学损伤明显，KL组细胞损伤明显减轻。结论CaMKⅡ参与了利多卡因诱发神经细胞的损伤。

英文摘要：

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ （CaMK Ⅱ ） in the neuronal damage induced by lidoeaine. Methods SH-SYSY cells were seeded in 96-well plates （100 μl/hole） with a density of 5 × 10^5/ml and randomly divided into 4 groups （ n = 63 each） ： normal culture group （C group）, CaMK Ⅱ inhibitor KN93 （K group）, lidocaine group （L group） and KN93 ＋ lidocaine group （KL group）. KN93 （final concentration 1 μmol/L） was added to the culture medium and the cells were then cultured for 24 h in group K. Lidocaine （final concentration 10 mmol/L） was added to the culture medium and the cells were then cultured for 24 h in group L. KN93 （final concentration 1 μmol/L） and lidocaine （final concentration 10 mmol/L） were added to the culture medium and the cells were then cultured for 24 h in group KL. The cell mor- phology was examined with microscope after 24 h of incubation. The viability of ceils was measured by MTT assay before incubation and at 1, 6, 12 and 24 h of incubation. The apoptosis in the cells was assessed by flow cytome- try. The apoptotic rate was calculated. Results Compared with C and K groups, the cell viability was significantly decreased and the apoptotic rate was increased in L and KL groups （ P 〈 0.05） . The cell viability was significantly higher and the apoptotic rate was lower in group KL than in group L （ P 〈 0.05） . There was no significant differ- ence in the cell viability and apoptotic rate between C group and K group （ P 〉 0.05） . The pathological changeswere obvious in group L and significantly reduced in group KL. Conclusion CaMK Ⅱ is involved in the neuronal damage induced by lidocaine.