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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。
OBJECTIVE: To investigate the changes of iron metabolism in mangine glycoside-induced daunomycin-induced myocardial toxicity in rats, and to study its mechanism. Methods: Cardiomyocytes were treated with 4μmol / L daunorubicin alone or in combination with 25 ~ 200μmol / L mangiferin for 24 hours, 48 hours and 72 hours. Cardiomyocytes were detected by qRT-PCR The mRNA expression of IRP1 and IRP2 were detected by RT-PCR, and the expression of Fn mRNA was detected by immunocytochemical staining. The expressions of IRP1 and transferrin Receptor (TfR) expression. Results: The expressions of IRP1 and IRP2 in mangiferin-treated group were lower than those in daunorubicin (4μmol / L) group at 25 ~ 200μmol / L for 24 hours. After intervention for 48 hours and 72 hours, Group; In 24 hours and 72 hours, the expression of Fn in mangiferin-treated group was lower than that in daunorubicin group at 25 ~ 200μmol / L, and increased after 48 hours intervention; The expression of Tf and TfR in Erythromycin group and 25 ~ 200μmol / L mangiferin model group were significantly higher than those in blank control group at 24 hours. TfR expression in Daunorubicin group at 72 hours was significantly lower than that in blank control group, while 25 ~ 200μmol / L mangiferin model group compared with daunorubicin group increased. CONCLUSION: Mangiferin can change the iron metabolism of daunorubicin-induced cardiomyocytes. It can be speculated that iron metabolism may be one of the mechanisms by which mangiferin protects daunomycin-induced cardiomyocyte toxicity in rats.