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目的观察晚期糖基化终末产物(AGEs)与其受体相互作用是否与K562及K562/A02细胞对阿霉素(ADM)耐药性相关。方法用流式细胞术检测K562及K562/A02细胞晚期糖基化终末产物受体(RAGE)及P-糖蛋白(P-gp)的表达和细胞凋亡率,CCK-8法观察AGEs对K562及K562/A02细胞增殖的影响,计算AGEs作用下两种细胞对ADM的半抑制浓度(IC50)值,用半定量RT-PCR检测mdr1mRNA相对表达水平。结果 K562与K562/A02细胞RAGE表达比较差异无统计学意义。AGEs可呈浓度和依赖性促进K562及K562/A02细胞增殖(P<0.05);AGEs作用K562及K562/A02细胞48h后,K562细胞mdr1mRNA及P-gp的表达均为阴性,K562/A02细胞mdr1mRNA及P-gp的表达与不加AGEs组比较差异均无统计学意义。结论 AGEs不能改变K562细胞对ADM的敏感性,同时亦不能改变K562/A02细胞对ADM的耐药性;AGEs与其受体相互作用与K562及K562/A02细胞耐药性无关。
Objective To investigate whether the interaction of advanced glycation end products (AGEs) with their receptors is related to ADM resistance in K562 and K562 / A02 cells. Methods Flow cytometry was used to detect the expression of advanced glycation end product receptor (RAGE) and P-glycoprotein (P-gp) and the apoptosis rate in K562 and K562 / A02 cells. The effects of AGEs on CCK-8 K562 and K562 / A02 cells. The half inhibitory concentrations (IC50) of ADM and ADM were calculated by using the two kinds of cells under the action of AGEs. The relative expression level of mdr1 mRNA was detected by semi-quantitative RT-PCR. Results There was no significant difference in RAGE expression between K562 and K562 / A02 cells. AGEs promoted the proliferation of K562 and K562 / A02 cells in a concentration-and-dependent manner (P <0.05). After AGEs treated K562 and K562 / A02 cells for 48h, the expressions of mdr1 mRNA and P-gp were negative in K562 / A02 cells There was no significant difference in the expression of P-gp between the two groups. CONCLUSION: AGEs can not change the sensitivity of K562 cells to ADM and do not change the resistance of K562 / A02 cells to ADM. The interaction of AGEs with its receptors has nothing to do with the drug resistance of K562 and K562 / A02 cells.