论文部分内容阅读
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 toxic effect of bupivacaine on mouse skeletal muscle cells and its mechanism. Methods C2C12 cells were stimulated with different concentrations of bupivacaine 100, 300, 600, 900 and 1200μmol / L, and another control group without drug. Cell viability was detected by MTT assay. Cell death was detected by cytotoxicity / cytotoxicity kit. Cell morphology was observed under optical microscope. The phosphorylation of Akt and p70S6K protein was detected by Western blot. Results Compared with the control group, bupivacaine decreased cell viability, induced cell death and down-regulated phosphorylation of Akt and p70S6K (P <0.05) in a concentration-dependent manner. Conclusion Bupivacaine has obvious toxic effect on skeletal muscle cells of mice; its mechanism may be related to the inhibition of Akt and p70S6K activity.