临床肿瘤学杂志
臨床腫瘤學雜誌
림상종류학잡지
CHINESE CLINICAL ONCOLOGY
2015年
5期
406-410
,共5页
去甲斑蝥素%白血病%细胞增殖%凋亡%细胞周期%NF-κB
去甲斑蝥素%白血病%細胞增殖%凋亡%細胞週期%NF-κB
거갑반모소%백혈병%세포증식%조망%세포주기%NF-κB
Norcantharidin%Leukemia%Proliferation%Apoptosis%Cell cycles%NF-κB
目的：探讨去甲斑蝥素（ NCTD）对白血病细胞系K562的增殖、凋亡、细胞周期及核因子（ NF）?κB活性的影响。方法采用CCK?8试剂盒检测不同浓度NCTD（0、10、25、50、100μmol／L）处理K562细胞24、48、72、96 h后的增殖抑制率，采用流式细胞术检测不同浓度NCTD处理24、48 h后的细胞凋亡率和处理48 h后的细胞周期，采用原位细胞凋亡检测试剂盒（ Tunnel）检测不同浓度NCTD处理24、48 h后的细胞凋亡指数，采用Western blotting检测不同浓度NCTD处理48 h后的NF?κB p65及IκB?α水平以评价NF?κB活性的变化。结果在10～100μmol／L范围内，NCTD可呈时间和浓度依赖的方式升高K562细胞的增殖抑制率，各浓度间的差异有统计学意义（ P＜0?05）；与0μmol／L相比，其余各浓度处理24、48 h后的凋亡率和凋亡指数均升高，处理48 h后的G0／G1期细胞比例升高，S、G2／M期细胞比例均降低，NF?κB p65水平降低，IκB?α水平升高，以上差异均有统计学意义（ P＜0?05）。结论 NCTD对白血病细胞系K562有细胞毒性，可抑制该细胞的增殖、诱导其凋亡及细胞周期阻滞并下调NF?κB表达。
目的：探討去甲斑蝥素（ NCTD）對白血病細胞繫K562的增殖、凋亡、細胞週期及覈因子（ NF）?κB活性的影響。方法採用CCK?8試劑盒檢測不同濃度NCTD（0、10、25、50、100μmol／L）處理K562細胞24、48、72、96 h後的增殖抑製率，採用流式細胞術檢測不同濃度NCTD處理24、48 h後的細胞凋亡率和處理48 h後的細胞週期，採用原位細胞凋亡檢測試劑盒（ Tunnel）檢測不同濃度NCTD處理24、48 h後的細胞凋亡指數，採用Western blotting檢測不同濃度NCTD處理48 h後的NF?κB p65及IκB?α水平以評價NF?κB活性的變化。結果在10～100μmol／L範圍內，NCTD可呈時間和濃度依賴的方式升高K562細胞的增殖抑製率，各濃度間的差異有統計學意義（ P＜0?05）；與0μmol／L相比，其餘各濃度處理24、48 h後的凋亡率和凋亡指數均升高，處理48 h後的G0／G1期細胞比例升高，S、G2／M期細胞比例均降低，NF?κB p65水平降低，IκB?α水平升高，以上差異均有統計學意義（ P＜0?05）。結論 NCTD對白血病細胞繫K562有細胞毒性，可抑製該細胞的增殖、誘導其凋亡及細胞週期阻滯併下調NF?κB錶達。
목적：탐토거갑반모소（ NCTD）대백혈병세포계K562적증식、조망、세포주기급핵인자（ NF）?κB활성적영향。방법채용CCK?8시제합검측불동농도NCTD（0、10、25、50、100μmol／L）처리K562세포24、48、72、96 h후적증식억제솔，채용류식세포술검측불동농도NCTD처리24、48 h후적세포조망솔화처리48 h후적세포주기，채용원위세포조망검측시제합（ Tunnel）검측불동농도NCTD처리24、48 h후적세포조망지수，채용Western blotting검측불동농도NCTD처리48 h후적NF?κB p65급IκB?α수평이평개NF?κB활성적변화。결과재10～100μmol／L범위내，NCTD가정시간화농도의뢰적방식승고K562세포적증식억제솔，각농도간적차이유통계학의의（ P＜0?05）；여0μmol／L상비，기여각농도처리24、48 h후적조망솔화조망지수균승고，처리48 h후적G0／G1기세포비례승고，S、G2／M기세포비례균강저，NF?κB p65수평강저，IκB?α수평승고，이상차이균유통계학의의（ P＜0?05）。결론 NCTD대백혈병세포계K562유세포독성，가억제해세포적증식、유도기조망급세포주기조체병하조NF?κB표체。
Objective To investigate the effect of norcantharidin ( NCTD) on proliferation, apoptosis, cell cycle and the ac?tivity of nuclear factor ( NF)?κB on human leukemia cell line K562. Methods The K562 cell was treated with different concentrations of NCTD ( 0, 10, 25, 50, 100μmol/L) and the proliferation inhibition rates were measured by CCK?8 kit at 24, 48, 72, 96 h post?treatment. The apoptotic rates at 24 and 48 h together with cell cycle at 48 h after NCTD treatments were evaluated via flow cytometry. The in situ cell death detection kit ( Tunnel) was applied to measure the levels of apoptosis at 24 and 48 h post?treatment. As for the activity of NF?κB, levels of p65 subunit of NF?κB and IκB?α were detected by Western blotting at 48 h post?treatment. Results NCTD in the range 10 to 100μmol/L could increase the proliferation inhibition rates on K562 cells in a dose?and time?dependent man?ner ( P<0?05) . In comparison with 0μmol/L NCTD, there were elevated apoptotic rates and indices at 24 and 48 h post?treatment ( P<0?05). The treatment with NCTD (10?100μmol/L) resulted in a higher proportion of cells within G0/G1phase but a lower proportion of cells within S and G2/M phases with significant differences than 0μmol/L ( P<0?05) . Reduced IκB?αbut elevated p65 subunit of NF?κB were observed only in 10?100 μmol/L NCTD ( P<0?05) . Conclusion NCTD exhibited cytotoxity on K562 cells, possibly by the inhibition of the cell proliferation, induction of apoptosis and down?regulation of the activity of NF?κB.
