【作者】 石泽延；

【导师】 彭志刚；

【作者基本信息】 广西医科大学 ， 血液内科， 2012， 硕士

【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。方法以柔红霉素单用或联合应用不同浓度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表达情况；应用RT-PCR法检测铁蛋白(Fn) mRNA表达情况；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)表达情况。结果1、25-200μ mol/L芒果甙模型组在干预24小时后铁调节蛋白1、铁调节蛋白2表达水平较柔红霉素组降低,干预48小时后,二者表达较柔红霉素组升高(P<0.05),干预72小时后,各浓度芒果甙模型组铁调节蛋白1表达较柔红霉素组下降,而铁调节蛋白2表达较柔红霉素组逐渐升高；2、干预24小时、72小时25-200μ mol/L芒果甙模型组铁蛋白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(P<0.05);3、柔红霉素组24、48小时的转铁蛋白、转铁蛋白受体表达均明显高于空白对照组；25-200μ mol/L芒果甙模型组24小时两者表达亦明显高于空白对照组,48小时则显著下降,低于柔红霉素组；72小时柔红霉素组的转铁蛋白受体表达明显低于空白对照组,而25-200μ mol/L芒果甙模型组表达较柔红霉素组逐渐升高(P<O.05)。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 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.更多还原