姜黄素减轻利多卡因诱导神经细胞毒性的机制与自噬的关系
Relationship between mechanism of curcumin reducing lidocaine-induced neurotoxicity and autophagy
秦冠伦 1邱颐 1王晓冬 1丁玉美1
作者信息
- 1. 内蒙古医科大学第二附属医院麻醉手术中心,呼和浩特 010000
- 折叠
摘要
目的 评价姜黄素减轻利多卡因诱导神经细胞毒性的机制与自噬的关系.方法 体外培养人神经母细胞瘤SH-SY5Y细胞至对数生长期,采用随机数字表法分为3组(n=12):空白对照组(C组)、利多卡因组(Lid组)、姜黄素+利多卡因组(Cur+Lid组).Cur+Lid组用含1.0 μmol/L姜黄素的完全培养基孵育24 h,其余组用新鲜培养基,相同条件下培养24 h.随后Lid组和Cur+Lid组更换为含4.0 mmol/L利多卡因的完全培养基孵育24 h,C组更换为新鲜培养基,相同条件下培养24 h.于孵育或培养结束后,采用CCK-8法检测细胞活力,MDC法检测自噬体水平,Western blot法检测细胞P62、微管相关蛋白轻链3-Ⅱ(LC3-Ⅱ)、LC3-Ⅰ的表达水平,计算LC3-Ⅱ/LC3-Ⅰ比值.结果 与C组相比,Lid组和Cur+Lid组细胞活力降低,自噬体水平升高,LC3-Ⅱ表达上调,LC3-Ⅰ表达下调,LC3-Ⅱ/LC3-Ⅰ比值升高,P62表达下调(P＜0.05);与Lid组相比,Cur+Lid组细胞活力升高,自噬体水平升高,LC3-Ⅱ表达上调,LC3-Ⅰ表达下调,LC3-Ⅱ/LC3-Ⅰ比值升高,P62表达下调(P＜0.05).结论 姜黄素减轻利多卡因诱导的神经细胞毒性的机制可能与激活自噬有关.
Abstract
Objective To evaluate the relationship between the mechanism of curcumin attenuating lidocaine-induced neurotoxicity and autophagy.Methods In vitro human neuroblastoma SH-SY5Y cells at the logarithmic phase were divided into 3 groups(n=12 each)using the random number table method:blank control group(C group),lidocaine group(Lid group),and curcumin+lidocaine group(Cur+Lid group).The cells were incubated with complete medium containing 1.0 μmol/L curcumin for 24 h,and the other groups were incubated with fresh medium for 24 h under the same conditions in Cur+Lid group.Then the medium was incubated with the complete medium containing 4.0 mmol/L lidocaine for 24 h in Lid and Cur+Lid groups,and the medium was replaced with the fresh medium and the cells were incubated for 24 h under the same conditions in group C.At the end of incubation or culture,the cell viability was detected by CCK-8 method,the level of autophagosomes was detected by the MDC method,and the expression of P62,microtubule-associated protein light chain 3-Ⅱ(LC3-Ⅱ)and LC3-Ⅰ was detected by Western blot,and the LC3-Ⅱ/LC3-Ⅰ ratio was calculated.Results Compared with group C,the cell viability was signifi-cantly decreased,the level of autophagosomes was increased,the expression of LC3-Ⅱ was up-regulated,the expression of LC3-Ⅰ was down-regulated,the LC3-Ⅱ/LC3-Ⅰ ratio was increased,and the expression of P62 was down-regulated in Lid and Cur+Lid groups(P＜0.05).Compared with Lid group,the cell viabil-ity and level of autophagosome were significantly increased,the expression of LC3-Ⅱ was up-regulated,the expression of LC3-Ⅰ was down-regulated,the LC3-Ⅱ/LC3-Ⅰ ratio was increased,and the expression of P62 was down-regulated in Cur+Lid group(P＜0.05).Conclusions The mechanism by which curcumin reduces the neurotoxicity induced by lidocaine may be related to the activation of autophagy.
关键词
姜黄素/自噬/利多卡因/神经元/药物相关性副作用和不良反应Key words
Curcumin/Autophagy/Lidocaine/Neurons/Drug-related side effects and ad-verse reactions引用本文复制引用
基金项目
内蒙古自治区高等学校科学研究项目(NJZZ22638)
出版年
2024
NETL
NSTL
万方数据