摘要
To explore the influence of reactive oxygen species (ROS) during heat shock on the activity of superoxide dismutase (SOD) and the endurance of cardiomyocytes against hypoxia reoxygenation damage Methods Cultured rat neonatal cardiomyocytes were divided into 5 groups (n=6/group): normal control, anoxic control, heat shock, heat shock + SOD (150?U/ml) and exogenous ROS pretreated Myocytes were first incubated in a CO 2 incubator (37℃) with Hank's solution for 30?min, followed by specific pretreatment Heat shock was performed by incubating the cells in a 43℃ incubator for 30?min; exogenous ROS were generated by the reaction of xanthine oxidase with xanthine After the dishes were returned to normal incubation conditions for 24?h, myocytes underwent hypoxia (3?h) and reoxygenation (1?h) Results Compared with control groups, ROS production increased after the cells experienced heat shock (1 28±0 34?nmol/mg·protein vs 0 80±0 23?nmol/mg·protein and 0 74±0 20?nmol/mg·protein, P <0 05) or ROS pretreatment (3 30±0 58?nmol/mg·protein, P <0 05) 24 hours later, accompanied by attenuated cellular injury, significantly increased SOD activity was found in heat shock (2 55±0 43?U/mg·protein vs 0 77±0 12?U/mg·protein and 0 63±0 09?U/mg·protein, P <0 05) and exogenous ROS pretreated (2 34±0 31?U/mg·protein, P <0 05) groups following reoxygenation Moreover, opposite results were found when myocytes were treated with SOD during heat shock Conclusions The release of ROS during heat shock triggers delayed myocardial protection by altering the activity of SOD ROS may play an important pathophysiological role in heat shock induced myocardial protection
To explore the influence of reactive oxygen species (ROS) during heat shock on the activity of superoxide dismutase (SOD) and the endurance of cardiomyocytes against hypoxia reoxygenation damage Methods Cultured rat neonatal cardiomyocytes were divided into 5 groups (n=6/group): normal control, anoxic control, heat shock, heat shock + SOD (150?U/ml) and exogenous ROS pretreated Myocytes were first incubated in a CO 2 incubator (37℃) with Hank's solution for 30?min, followed by specific pretreatment Heat shock was performed by incubating the cells in a 43℃ incubator for 30?min; exogenous ROS were generated by the reaction of xanthine oxidase with xanthine After the dishes were returned to normal incubation conditions for 24?h, myocytes underwent hypoxia (3?h) and reoxygenation (1?h) Results Compared with control groups, ROS production increased after the cells experienced heat shock (1 28±0 34?nmol/mg·protein vs 0 80±0 23?nmol/mg·protein and 0 74±0 20?nmol/mg·protein, P <0 05) or ROS pretreatment (3 30±0 58?nmol/mg·protein, P <0 05) 24 hours later, accompanied by attenuated cellular injury, significantly increased SOD activity was found in heat shock (2 55±0 43?U/mg·protein vs 0 77±0 12?U/mg·protein and 0 63±0 09?U/mg·protein, P <0 05) and exogenous ROS pretreated (2 34±0 31?U/mg·protein, P <0 05) groups following reoxygenation Moreover, opposite results were found when myocytes were treated with SOD during heat shock Conclusions The release of ROS during heat shock triggers delayed myocardial protection by altering the activity of SOD ROS may play an important pathophysiological role in heat shock induced myocardial protection
