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目的探讨醛糖还原酶相似基因-1(ARL-1基因)与人肝癌细胞耐药性的关系。方法线性化的ARL-1表达载体DNA转染至人肝癌细胞系(HepG-2细胞)作为实验组。含有活性醛基的表阿霉素、丝裂霉素作为实验用药,不含活性醛基的氟尿嘧啶作为阳性对照。通过乳酸脱氢酶(LDH)的测定、MTT法和流式细胞仪研究ARL-1基因在肝癌细胞耐药性形成中的作用。结果ARL-1基因成功转染至人肝癌细胞HepG-2,加入表阿霉素和丝裂霉素后,实验组的细胞毒性水平和细胞凋亡率明显低于对照组(P<0·05),耐药水平明显上升。加入氟尿嘧啶后,实验组及对照组的耐药水平无明显差异。结论高表达的ARL-1基因明显降低含有活性醛基化疗药物的细胞毒性和抑制其所诱导的细胞凋亡,增强人肝癌细胞的耐药性。
Objective To investigate the relationship between the aldose reductase similar gene-1 (ARL-1) gene and the drug resistance of human hepatoma cells. Methods The linearized ARL-1 expression vector DNA was transfected into human hepatoma cell line (HepG-2 cells) as experimental group. Epirubicin containing active aldehyde groups, mitomycin as experimental drugs, and fluorouracil without active aldehyde groups were used as positive control. The effect of ARL-1 gene on the drug resistance of hepatocellular carcinoma cells was studied by the determination of lactate dehydrogenase (LDH), MTT assay and flow cytometry. Results The ARL-1 gene was successfully transfected into HepG-2 cells. After addition of epirubicin and mitomycin, the cytotoxicity and apoptosis rate of the experimental group were significantly lower than those of the control group (P <0.05) ), Drug resistance increased significantly. After adding fluorouracil, the experimental group and the control group no significant difference in drug levels. Conclusion The high expression of ARL-1 gene significantly reduces the cytotoxicity of active aldehyde-containing chemotherapy drugs and inhibits the apoptosis induced by it, and enhances the drug resistance of human hepatoma cells.