论文部分内容阅读
目的观察苯代谢物对K562细胞转铁蛋白受体表达的影响以及DNA甲基化抑制剂5-氮杂-2’-脱氧胞苷的干预作用。方法 K562细胞用苯代谢物处理72 h,处理期间的后48 h加入5-氮杂-2’-脱氧胞苷进行干预,然后利用荧光标记抗体结合流式细胞技术分析细胞表面转铁蛋白受体的表达,应用半定量反转录PCR技术分析细胞转铁蛋白受体mRNA的表达水平。结果苯代谢物苯酚(200~800μmol/L)、氢醌(10~40μmol/L)和1,2,4-苯三醇(5~20μmol/L)均能浓度和时间依赖性抑制转铁蛋白受体在细胞表面的表达和浓度依赖性抑制细胞内转铁蛋白受体mRNA表达;而5-氮杂-2’-脱氧胞苷可显著拮抗苯代谢物抑制转铁蛋白受体表达的作用。结论苯代谢物可抑制红系祖细胞转铁蛋白受体的表达,而DNA甲基化可能参与其中,转铁蛋白受体的表达抑制会影响细胞铁的摄入,从而影响血红素合成,继而抑制血红蛋白合成影响红系分化。
Objective To observe the effects of benzene metabolites on the expression of transferrin receptor in K562 cells and the intervention of 5-aza-2’-deoxycytidine, a DNA methylation inhibitor. METHODS K562 cells were treated with benzene metabolites for 72 h and 5-aza-2’-deoxycytidine was added 48 h after treatment. Fluorescent labeled antibody combined with flow cytometry was used to analyze the cell surface transferrin receptor The expression of transferrin receptor mRNA was analyzed by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Results The benzene metabolites (200-800μmol / L), hydroquinone (10-40μmol / L) and 1,2,4-benzenetriol (5-20μmol / L) inhibited the concentration and time- Receptor on the cell surface expression and concentration-dependent inhibition of intracellular transferrin receptor mRNA expression; and 5-aza-2’-deoxycytidine significantly antagonized benzene metabolites inhibit transferrin receptor expression. Conclusion Benzene metabolites can inhibit the expression of transferrin receptor in erythroid progenitor cells, and DNA methylation may participate in them. Inhibition of transferrin receptor expression may affect the uptake of cellular iron and thus hemoglobin synthesis, which in turn Inhibition of Hemoglobin Synthesis Affects Erythroid Differentiation.