Role of calcium/calmodulin-dependent protein kinase Ⅱ in neuronal damage induced by lidocaine
10.3760/cma.j.issn.0254-1416.2012.11.014
- VernacularTitle:钙/钙调素依赖性蛋白激酶Ⅱ在利多卡因诱发神经细胞损伤中的作用
- Author:
Xianjie WEN
;
Shiyuan XU
;
Hua LIANG
;
Qingguo ZHANG
;
Xueqin ZHENG
;
Hongzhen LIU
;
Hanbing WANG
;
Chengxiang YANG
- Publication Type:Journal Article
- Keywords:
Calcium-calmodulin-dependent protein kinase type 2;
Lidocaine;
Drug toxicity
- From:
Chinese Journal of Anesthesiology
2012;(11):1337-1339
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the neuronal damage induced by lidocaine.Methods SH-SY5Y cells were seeded in 96-well plates (100 μl/hole) with a density of 5 × 105/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 morphology was examined with microscope after 24 h of incubation.The viability of cells 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 cytometry.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 difference in the cell viability and apoptotic rate between C group and K group (P ＞ 0.05).The pathological changes were obviousin group L and significantly reduced in group KL.Conclusion CaMK Ⅱ is involved in the neuronal damage induced by lidocaine.
