Ilexonin A Induced Apoptosis Of Leukemia Cell K562and Survivin、Bax MRNA Effect

Objective:To investigate the role and mechanism of the inbibitional effect of IA on the proliferation of leukemia cell K562.Methods:1.Culture K562cell, subculture every2-3days, select Logarithmic growth phase cells as experimental subject.2.Explore the inbibitional effect of IA on the concentration and action time of growth activity of K562by MTT method.Implant cells with Ilexonin, set five concentration gradients:0.8.0.4.0.2.0.1.0.05g/mL; set blank control group, four hole in each group, which continues to develop24,48,72hours, determine the impact of ilexonin on the activity of cell growth by MTT method.3.Detect the expression of Survivin Bax gene with RT-PCR method.Select intervention cells.of each phase Separately.Extracted the mRNA of each phase cells, using reverse transcription techniques, synthesis cDNA of each phase cells, through the design of Survivin Bax gene primers, amplification Survivin Bax gene sequences by PCR,take β-actin as the beta-actin genes,use software to detect the expression of Survivin. Bax gene in intervention cells.of each phase4.Statistical analysisSPSS17.0software analysis,the date is expressed by mean () standard deviation,correlated samples nonparametric analysis,P<0.05show difference has statistical significance,P＞0.05show difference has not statistical significance.Results:1.Ilexonin restrain multiplication of K562cell line which presenting dependece of time and dosage. The growing of K562cell present obviously inhibitional effect which dealed with by0.4mg/mL ilexonin after72hour.2.Cells could present morphological changes of apoptosis after dealed with by ilexonin, the volume of a fraction of cells change samll,chromatin present concentration and edge set.3.The RT-PCR way and the testing result of flow cytometry assume ilexonin could retrain Survivin’up-regulation and promote Bax’express.Conclusion:l.Ilexonin restrain the multipliction of K562cells,assuming the dependence of time and dosage.2.It is the probable molecular mechanism of ilexonin’ which resisting the leukemia cell that restrain the multiplication or promoting the apoptosis of K562cells by regulate the express of Survivin and Bax.