布比卡因对小鼠骨骼肌细胞的毒性作用  

Cytotoxicity of bupivacaine on mouse skeletal muscle cells

作　　者：毛雨[1] 赵艳林[1] 熊静薇 李荣荣[2] 刘莉[1] 

机构地区：[1]南京师范大学生命科学院,江苏省210046 [2]南京医科大学第一附属医院麻醉科

出　　处：《江苏医药》2015年第7期745-746,F0002,共3页Jiangsu Medical Journal

基　　金：国家自然科学基金(81370260)

摘　　要：目的探讨布比卡因对小鼠骨骼肌细胞的毒性作用及其作用机制。方法用不同浓度布比卡因100、300、600、900、1200μmol/L刺激C2C12细胞;另设不加药物的对照组。采用MTT法检测细胞活力,细胞活性/细胞毒性试剂盒检测细胞死亡,光学显微镜下观察细胞形态,Western blot检测Akt和p70S6K蛋白的磷酸化水平。结果与对照组相比,布比卡因呈浓度依赖性地降低细胞存活率,诱导细胞死亡,并下调Akt和p70S6K蛋白的磷酸化水平(P<0.05)。结论布比卡因对小鼠骨骼肌细胞具有明显的毒性作用;其机制可能与抑制Akt和p70S6K活性有关。Objective To investigate the cytotoxicity and underlying mechanism of bupivacaine on mouse skeletal muscle cells.Methods C2C12 cells were stimulated by bupivacainewith in different concentrations of 100,300,600,900 and 1200μmol/L.C2C12 cells without any stimulation were taken as the controls.The cell viability and death were determined by MTT assay and Live/Dead kit,respectively.The cell morphology was observed under optical microscope,and the phosphorylation levels of Akt and p70S6 K were detected by Western blot.Results Compared with control group,bupivacaine significantly decreased cell viability in a dose-dependent manner,promoted cell death,and downregulated the phosphorylation levels of Akt and p70S6K（P〈0.05）.Conclusion Bupivacaine obviously induces cytotoxicity,probably via inactivation of Akt/p70S6 Ksignaling pathway in mouse skeletal muscle cells.

关 键 词：布比卡因 骨骼肌细胞 细胞毒性 

分 类 号：R685[医药卫生—骨科学]