【摘要】 目的:探讨铁代谢在芒果甙保护柔红霉素致大鼠心肌毒性细胞中的改变,并对其作用机制进行初步研究。方法:以4μmol/L柔红霉素单用或联合应用25～200μmol/L芒果甙为处理因素作用于大鼠心肌细胞24小时、48小时及72小时,应用qRT-PCR法检测各组心肌细胞铁调节蛋白1(IRP1)、铁调节蛋白2(IRP2)mRNA表达,应用RT-PCR法检测铁蛋白(Fn)mRNA表达,同时采用免疫细胞化学染色法检测转铁蛋白(Tf)及转铁蛋白受体(TfR)表达。结果:25～200μmol/L芒果甙模型组在干预24小时后IRP1、IRP2表达水平较柔红霉素(4μmol/L)组降低,干预48小时、72小时后,二者表达较柔红霉素组升高;干预24小时、72小时25～200μmol/L芒果甙模型组Fn表达较柔红霉素组随浓度升高逐渐降低,干预48小时后则较柔红霉素组均升高;柔红霉素组及25～200μmol/L芒果甙模型组24小时的Tf、TfR表达均明显高于空白对照组;72小时柔红霉素组的TfR表达明显低于空白对照组,而25～200μmol/L芒果甙模型组表达较柔红霉素组升高。结论:芒果甙能改变柔红霉素心肌毒性细胞的铁代谢水平,由此可推测,铁代谢可能是芒果甙保护柔红霉素致大鼠心肌细胞毒性的机制之一。更多还原

【Abstract】 Objective: To study the changes of iron metabolism in the mangiferin protection of daunorubicin induced rat myocardial toxicity cell,and investigate its preliminary mechanism.Methods: With 4μmol / L daunorubicin alone or combined application of 25 ～ 200μmol / L concentrations of mangiferin for processing factors acting on rat myocardial cells of 24h,48h and 72h,application of qRT-PCR assay for the detection of myocardial cells in each group of iron regulatory protein 1(IRP1),iron regulatory protein 2(IRP2) mRNA expression,application of RT-PCR method for the detection of ferritin(Fn) mRNA expression,while the use of immunocytochemical staining method for the detection of transferrin(Tf) and transferrin receptor(TfR) expression.Results: ①The 25 ～ 200μmol / L concentrations of mangiferin model groups intervented in 24h both decreased the expression levels compared with the negative control group,while in the intervention of 48h,72h,compared with the daunorubicin group(4μmol / L) elevated expression.②The intervention of 24h、72h,25 ～ 200μmol / L concentrations of mangiferin model group compared with the daunorubicin group expression gradually decreased,but all higher than the daunorubicin group in 48h.③With the daunorubicin group and the 25 ～ 200μmol/L concentrations of mangiferin model groups in 24h,the transferrin expression of transferrin receptor were significantly higher than those in blank control group.Transferrin receptor expression of the daunorubicin group in 72h was significantly lower than those in blank control group,but the expression 25 ～ 200μmol / L concentrations of mangiferin model group compared with daunorubicin group rose.Conclusion: Mangiferin can change the iron metabolism level of daunorubicin myocardial toxicity cells.Which can be assumed,iron metabolism may be one of the mechanisms for mangiferin protection of rat myocardial cells induced by daunorubicin toxicity.更多还原