中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2014年
22期
6405-6407
,共3页
邓守恒%蔡晓军%潘东风%李芳%李林均%陈萍
鄧守恆%蔡曉軍%潘東風%李芳%李林均%陳萍
산수항%채효군%반동풍%리방%리림균%진평
硒化壳聚糖%K562/ADM细胞%多药耐药%生物学行为
硒化殼聚糖%K562/ADM細胞%多藥耐藥%生物學行為
서화각취당%K562/ADM세포%다약내약%생물학행위
Selenium chiston%K562/ADM cells%Multidrug resistance%Biological behaviour
目的:观察硒化壳聚糖对体外培养慢性粒细胞多药耐药白血病细胞株 K562/阿霉素( ADM)细胞生物学行为的影响。方法硒化壳聚糖作用于体外培养的K562/ADM细胞12、24 h,应用流式细胞法检测细胞凋亡,软件拟合计算细胞周期;应用免疫印迹法检测P-糖蛋白( P-gp)的表达;应用RT-PCR法检测MDR-1 mRNA水平。结果硒化壳聚糖能够明显增强 ADM对 K562/ADM细胞的诱导凋亡作用,阻滞细胞周期于 G1期(P<0.05,P<0.01),下调P-gp表达和MDR-1 mRNA水平(P<0.05,P<0.01),硒化壳聚糖浓度越高,作用效果越显著。结论硒化壳聚糖能够通过下调MDR-1基因和P-gp表达,阻滞细胞周期于G1期来诱导细胞凋亡,进而对体外培养的K562/ADM细胞耐药生物学行为产生逆转。
目的:觀察硒化殼聚糖對體外培養慢性粒細胞多藥耐藥白血病細胞株 K562/阿黴素( ADM)細胞生物學行為的影響。方法硒化殼聚糖作用于體外培養的K562/ADM細胞12、24 h,應用流式細胞法檢測細胞凋亡,軟件擬閤計算細胞週期;應用免疫印跡法檢測P-糖蛋白( P-gp)的錶達;應用RT-PCR法檢測MDR-1 mRNA水平。結果硒化殼聚糖能夠明顯增彊 ADM對 K562/ADM細胞的誘導凋亡作用,阻滯細胞週期于 G1期(P<0.05,P<0.01),下調P-gp錶達和MDR-1 mRNA水平(P<0.05,P<0.01),硒化殼聚糖濃度越高,作用效果越顯著。結論硒化殼聚糖能夠通過下調MDR-1基因和P-gp錶達,阻滯細胞週期于G1期來誘導細胞凋亡,進而對體外培養的K562/ADM細胞耐藥生物學行為產生逆轉。
목적:관찰서화각취당대체외배양만성립세포다약내약백혈병세포주 K562/아매소( ADM)세포생물학행위적영향。방법서화각취당작용우체외배양적K562/ADM세포12、24 h,응용류식세포법검측세포조망,연건의합계산세포주기;응용면역인적법검측P-당단백( P-gp)적표체;응용RT-PCR법검측MDR-1 mRNA수평。결과서화각취당능구명현증강 ADM대 K562/ADM세포적유도조망작용,조체세포주기우 G1기(P<0.05,P<0.01),하조P-gp표체화MDR-1 mRNA수평(P<0.05,P<0.01),서화각취당농도월고,작용효과월현저。결론서화각취당능구통과하조MDR-1기인화P-gp표체,조체세포주기우G1기래유도세포조망,진이대체외배양적K562/ADM세포내약생물학행위산생역전。
Objective To investigate the effect of Selenium chiston (Sc) on biological behaviour of human leukemia multidrug re-sistance cell line K562/ADM in vitro.Methods After treated with Sc for 12,24 h,the apoptosis rate and cell phase in K 562/ADM were ex-amined by flow cytometry.Expression of P glycoprotein ( P-gp) in K562/ADM was determined by Western blot and transcription level of MDR-1 gene was detected by semi-quantitative RT-PCR.Results Sc could obviously enhance the inducing effect of ADM on apoptosis of K562/ADM cell and block cell cycle into G1 phase(P<0.05,P<0.01),down-regulate the P-gp and MDR-1 mRNA level in K562/ADM cell ( P<0.05 ,P<0.01 ) in a dose and time dependent manner .Conclusions Sc could change the biological behaviour of K 562/ADM cell in vitro through enhancing cell apoptosis ,blocking cell cycle in G1 phase,inhibiting the P-gp and MDR-1 gene expression.