Effect of gangliosides pretreatment on expression of caspase-3 in apoptosis of mouse neuroblastoma Neu-ro2a induced by bupivacaine / 临床麻醉学杂志

ABSTRACT

Objective To discuss the impact of the neurotoxity of bupivacaine and bupivacaine-induced cellular neurotoxicity caused by pretreatment of ganglion (GM-1 )monoglyceride on the ex-pression of caspase-3.Methods The mouse neuroblastoma cells-N2a cells was used as a research object to carry out the following experiments(1)To observe the damage effects of different concen-trations of bupivacaine on N2a cells and find out the most suitable damage concentration to establish cell damage model.The N2a cells were interacted with bupivacaine with different concentrations [0μmol/L (group C),600 μmol/L (group B1),900 μmol/L (group B2),1 200 μmol/L (group B3), 1 500 μmol/L (group B4),2 000 μmol/L (group B5)]for 6,12,24,36 h and then evaluated by CCK-8 cell survival.Each experiment was repeated three times.The protective function of GM-1 to bupiva-caine-induced N2a cells damage.The N2a cells were treated with different concentrations (0.1μmol/L (group BG1),1.0 μmol/L (group BG2),10 μmol/L (group BG3))of GM-1 pretreatment 24 h,CCK-8 was evaluated in cell viability,Western Blot method was used to detect damaged cells caspase-3 expression levels.Each experiment was repeated three times.Results (1)Bupivacaine could significantly damage N2a cells,the greater the bupivacaine concentration,the longer the action time,the stronger neurotoxicity.(2)GM-1 bupivacaine nerve injury had a significant protective effect in a dose-related manner.The maximum of protective dose of this experiment was 10 μmol/L.Conclusion Bupivacaine can significantly damage N2a cells,correlating with both dose and time double positively,while GM-1 pretreatment significantly reduced the expression of caspase-3 induced by bupivacaine.