摘要
目的:研究三氧化二砷(arsenic trioxide,ATO)对K562/A02细胞表达血管内皮生长因子(vascular endo- thelial growth factor,VEGF)和P-糖蛋白(P-glycoprotein,P-gP)的影响,并对VEGF和P-gp的相关性进行探讨。方法:用甲基噻唑基四唑(MTT)法检测ATO对K562/A02细胞的增殖抑制率,酶联免疫吸附双抗体夹心法(enzyme-linked immunosorbent assay,ELISA)测定上清VEGF含量,流式细胞术测定P-gP表达率。结果:0.05μmol/L ATO对K562/A02细胞的增殖和VEGF的表达无明显影响;0.4、3.2μmol/L ATO则对K562/A02细胞有明显的增殖抑制作用和下调VEGF的作用(P<0.05)。P-gP经0.05、0.4μmol/L ATO处理24、48、72h后无明显变化(P>0.05),3.2μmol/L ATO处理48、72 h后可显著下调P-gP表达(P<0.05)。结论:ATO逆转K562/A02细胞多药耐药(multidrug resistance,MDR)的作用可能与其调控P-gP和VEGF的水平有关;K562/A02细胞VEGF水平与P-gP的表达率可能有一定的相关性。
Objective： To investigate the effects of arsenic trioxide （ATO） on the expressions of vascular endothelial growth factor （VEGF） and P-glycoprotein （P-gp） in K562/A02 cells and to explore the correlation between VEGF and P-gp. Methods： The inhibition rate of K562/A02 cell proliferation was detected by using methyl thiazolyl tetrazolium assay （MTT）; the level of VEGF was detected by enzyme-linked immunosorbent assay （ELISA） and the expression rate of P-gp was determined by flow cytometry （FCM）. Results： 0. 05 μmol/L ATO had no influences on the cell proliferation and the expression of VEGF in K562/A02 cells; 0.4 and 3.2 μmol/L ATO could significantly inhibit the K562/A02 cell proliferation and down-regulate the expression of VEGF in K562/A02 cells （P〈0. 05）. The expression of P-gp did not changed after being exposed to 0.05 and 0.4 μmol/L ATO for 24, 48 and 72 hours （P〈0.05）. 3.2 μmol/L ATO could remarkably reduce the expression of P-gp in K562/A02 cells after 48- and 72-hour incubation with ATO （P〈0.05）. Conclusions： The down-regulation of P-gp and VEGF after being exposed to ATO probably contributes to the reversion of multidrug resistance in K562/A02 cells. The level of VEGF may be related to the expression rate of P-gp in K562/A02 cells.
出处
《中西医结合学报》
CAS
2007年第6期647-650,共4页
Journal of Chinese Integrative Medicine
关键词
血管内皮
内皮生长因子
砷化合物
白血病
vascular endothelium
endothelial growth factors
arsenic compounds
leukemia
