Mangiferin On Soft Erythromycin Caused By Inhibition Of Myocardial Cell Apoptosis In Rats

Objective:The objective of this study is to investigate whether mangiferin can have a beneficial effect on daunorubicin-induced cardiac toxicity in vitro.Methods:Primary cultured neonatal rat cardiomyocytes were pretreated with daunorubicin (1μmol/L) to create the apoptosis model, then treated with different concentrations of mangiferin (25,50or100μmol/L). Ginkgo Biloba extract761(25μg/ml) was selected as positive control. We observed morphological changes of apoptosis, using the optic inverted microscope and electron microscope, and using flow cytometry (Annexin V-FITC/PI double staining) to count the rate of apoptosis, using spectrophotometry to detect Caspase-3activity in cell lysate, using real-time fluorescent quantitative RT-PCR to detect the expression of P53, Fas and FasL.Results:1、When treated with daunorubicin(1μmol/L), electron microscopic evidence of nuclei fragmentation with intact plasma membranes, and mangiferin could reduce cardiac cell destruction effectively.2、Mangiferin could significantly suppress the daunorubicin-induced myocardial apoptosis after effect on daunorubicin-induced apoptosis model. As the raise of the drug concentration, the effect of inhibition was increased and myocardial apoptosis was decreased. 3、After treatment with daunorubicin the expression of Fas and FasL gene in cardiomyocytes increased. With the concentration rise up, mangiferin could down-regulate the mRNA expression of Fas and FasL,4、Daunorubicin that activates effecter Caspase-3will potentially lead to apoptosis. Mangiferin proved protects cardiac cells is by inhibit Caspase-3activation. This had shown as a dose-dependent effect.Conclusion:Mangiferin can inhibit the daunorubicin-induced myocardial apoptosis. The mechanism at least partially associated with reducing the levels of Fas and FasL mRNA expression and inhibiting Caspase-3activation.