亚硒酸钠对K562/ADR细胞系VEGF表达的影响

Effects of Na_2SeO_3 on Expression of VEGF in K562/ADR Cells

为了探讨亚硒酸钠对K562/ADR细胞VEGF表达的影响,分别以5、10μmol/L的亚硒酸钠对培养的K562及K562/ADR细胞进行处理,应用ELISA法检测亚硒酸钠处理前和处理后不同时间的K562及K562/ADR细胞上清液中VEGF含量,用MTT法检测逆转耐药倍数。结果表明:亚硒酸钠可以增加K562/ADR细胞对阿霉素的敏感性,其逆转耐药的倍数为3.48倍;两种细胞系分泌的VEGF含量随培养时间的延长增加,并且各个时间段的K562/ADR细胞VEGF表达均高于K562细胞(P<0.05);5、10μmol/L的亚硒酸钠在72小时内均不能抑制K562细胞VEGF的分泌(P>0.05);而作用96小时时K562细胞上清液中VEGF水平虽有下降,但未达统计学意义;5、10μmol/L的亚硒酸钠在48小时内均不能抑制K562/ADR细胞VEGF的分泌(P>0.05),10μmol/L的亚硒酸钠在作用72和96小时可以明显抑制VEGF的分泌(P<0.001),5μmol/L的亚硒酸钠在作用96小时可以抑制VEGF的分泌(P<0.001)。结论:VEGF可能与白血病多药耐药有关,而亚硒酸钠则能抑制白血病细胞分泌VEGF。

In order to investigate the effects of Na2SeO3 on expression of VEGF in K562/ADR cells, K562 and K562./ ADR cells were treated with Na2SeO3 at dose of 5 and 10 μmol/L. The expressions of VEGF in K562 and K562/ADR cells were detected by ELISA before and at the different time point after treatment. The mutiplie of reversion of resistance was detected by MTT method. The results showed that Na2SeO3 at dose of 10 μmol/L could increase the sensitivity of K562/ADR cell to adriamycin, the multiple of reversion was 3.48. The expression levels of VEGF in K562 and K562/ADR cells increased with prolongation of time cultured, and the VEGF expression levels in K562/ADR cells at the different time points were higher than that in K562 cells （ P 〈0.05 ） ; 5 and 10 μmol/L Na2SeO3 did not suppress expression of VEGF in K562 cells at 72 hours （P 〉 0. 05 ）, and the VEGF level in K562 cells at 96 hours decreased without statistical significance; 5 and 10 μmol/L Na2SeO3 acting for 48 hours did not show suppressive effect on expression of VEGF in K562/ADR cells （ P 〉 0.05 ）, 5 μmol/ L Na2SO3 could decrease the expression of VEGF in K56Z/ADR cell after treatment for 96 hours, while 10 μmol/L Na2SeO3 could significantly decrease the expression of VEGF in K562/ADR cells treated for 72 hours and 96 hours （ P 〈0.01 ）. It is concluded that VEGF would be involved in the multidrug resistance of leukemia. Na2SeO3 decreasing expression of VEGF in leukemic cells may be one of the mechanisms reversing multidrug resistance.