Abstract: AIM: To investigate protective effect of propofol on the cytotoxicity of bupivacaine in pheochromocytoma PC12 cells of rat and role of endogenous thioredoxin (Trx) system.METHODS: The PC12 cells were inoculated and cultured on the culture capsule.The cultured PC12 cells were randomly assigned to one of four groups (n =6 holes each):Control group, bupivacaine group (B), propofol group (P) and bupivacaine combined with propofol group (BP).Survival rate of PC12 cells (%) treated with different drugs for 6 and 24 h induced was analyzed by MTT assay.Lactate dehydrogenase (LDH) in the culture medium was measured by spectroscopy.Thioredoxin reductase (TrxR) and ROS activities in the PC12 cells were assayed by spectrophotometer.The expression levels of Trx mRNA and TrxR mRNA were determined by RT-PCR.RESULTS: Compared with normal PC12 cells, bupivacaine significantly reduced the relative survival rate (P <0.01) and TrxR activity of the PC12 cells (P <0.05), markedly increased level of LDH in the culture medium(P <0.05) and ROS activity in the PC12 cells (P <0.01), and significantly decreased the expression of Trx mRNA and TrxR mRNA (P <0.05). Compared with B group, the relative survival rate of the PC12 cells were significantly increased (P <0.01) and TrxR activity of the PC12 cells were increased (P < 0.05);The level of LDH in the culture medium(P < 0.05) and ROS activity in the PC12 cells markedly decreased (P <0.01);The expression of Trx mRNA and TrxR mRNA was significantly increased (P <0.05) in PB group compared with those in B group.CONCLUSION: Bupivacaine induces cytotoxicity in the PC12 cell line, which may be associated with ROS production and decrease in TrxR activity.Propofol can prevent cytotoxicity of PC12 cells induced by bupivacaine, and one of the mechanisms may be associated with protecting endogenous thioredoxin system and scavenging ROS production.

Key words: bupivacaine, toxcity, propofol, PC12 cells, thioredoxin