Mangiferin In The Protection Of Rat Myocardial Cells Induced By Daunorubicin Toxicity Of Iron Metabolism Changes And Its Mechanism Research

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 With4μmol/L daunorubicin alone or combined application of25-200μmol/L concentrations of mangiferin for processing factors acting on rat myocardial cells of24h,48h and72h, application of qRT-PCR assay for the detection of myocardial cells in each group of iron regulatory protein1(IRP1), iron regulatory protein2(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. Results1、The25-200μmol/L concentrations of mangiferin model groups intervented in24h both decreased the expression levels compared with the negative control group, while in the intervention of48h,72h, compared with the daunorubicin group elevated expression (P<0.05)2、The intervention of24h、72h,25-200μmol/L concentrations of mangiferin model group compared with the daunorubicin group expression gradually decreased, but all higher than the daunorubicin group in48h(P<0.05).3、With the daunorubicin group and the25-200μmol/L concentrations of mangiferin model groups in24h, the transferrin expression of transferrin receptor were significantly higher than those in blank control group. Transferrin receptor expression of the daunorubicin group in72h was significantly lower than those in blank control group, but the expression25-200μmol/L concentrations of mangiferin model group compared with daunorubicin group rose (P<0.05)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.