白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2013年
3期
154-156,160
,共4页
孙启鑫%温真真%朱志刚%陈桂萍
孫啟鑫%溫真真%硃誌剛%陳桂萍
손계흠%온진진%주지강%진계평
白血病%老年人%硼替佐米%细胞增殖%细胞凋亡
白血病%老年人%硼替佐米%細胞增殖%細胞凋亡
백혈병%노년인%붕체좌미%세포증식%세포조망
Leukemia%Aged%Bortezomib%Cell proliferation%Cell apoptosis
目的 研究硼替佐米(Bor)对老年白血病患者原代细胞增殖、凋亡及其bcl-2家族蛋白表达的影响.方法 四甲基偶氮唑蓝(MTT)比色法检测细胞增殖活力；荧光显微镜形态观察、流式细胞术检测细胞凋亡；Western blot检测bcl-2、Bax蛋白表达.结果 50 ～ 5000 nmol/LBor均可抑制细胞增殖并诱导细胞凋亡,其中50 nmol/L和5000 nmol/L处理细胞24 h,细胞增殖活力分别下降至90％和70％,细胞凋亡率分别为(10.2±2.3)％和(13.3±3.3)％；延长处理时间至48 h,细胞活力进一步下降至86％和60％,细胞凋亡率增至(18.4±3.9)％和(20.7±3.7)％,与0 nmol/L Bor对照组相比差异均有统计学意义(F=53.76、F=7.74、F=54.49、F=16.94,均P＜ 0.05)；50 ～ 5000 nmol/L Bor处理细胞24、48 h,bel-2蛋白表达逐渐下降,Bax蛋白表达逐渐增加.结论 Bor对老年白血病患者原代细胞具有抑制增殖、诱导凋亡作用,其作用机制可能与bcl-2家族蛋白的表达水平变化相关.
目的 研究硼替佐米(Bor)對老年白血病患者原代細胞增殖、凋亡及其bcl-2傢族蛋白錶達的影響.方法 四甲基偶氮唑藍(MTT)比色法檢測細胞增殖活力；熒光顯微鏡形態觀察、流式細胞術檢測細胞凋亡；Western blot檢測bcl-2、Bax蛋白錶達.結果 50 ～ 5000 nmol/LBor均可抑製細胞增殖併誘導細胞凋亡,其中50 nmol/L和5000 nmol/L處理細胞24 h,細胞增殖活力分彆下降至90％和70％,細胞凋亡率分彆為(10.2±2.3)％和(13.3±3.3)％；延長處理時間至48 h,細胞活力進一步下降至86％和60％,細胞凋亡率增至(18.4±3.9)％和(20.7±3.7)％,與0 nmol/L Bor對照組相比差異均有統計學意義(F=53.76、F=7.74、F=54.49、F=16.94,均P＜ 0.05)；50 ～ 5000 nmol/L Bor處理細胞24、48 h,bel-2蛋白錶達逐漸下降,Bax蛋白錶達逐漸增加.結論 Bor對老年白血病患者原代細胞具有抑製增殖、誘導凋亡作用,其作用機製可能與bcl-2傢族蛋白的錶達水平變化相關.
목적 연구붕체좌미(Bor)대노년백혈병환자원대세포증식、조망급기bcl-2가족단백표체적영향.방법 사갑기우담서람(MTT)비색법검측세포증식활력；형광현미경형태관찰、류식세포술검측세포조망；Western blot검측bcl-2、Bax단백표체.결과 50 ～ 5000 nmol/LBor균가억제세포증식병유도세포조망,기중50 nmol/L화5000 nmol/L처리세포24 h,세포증식활력분별하강지90％화70％,세포조망솔분별위(10.2±2.3)％화(13.3±3.3)％；연장처리시간지48 h,세포활력진일보하강지86％화60％,세포조망솔증지(18.4±3.9)％화(20.7±3.7)％,여0 nmol/L Bor대조조상비차이균유통계학의의(F=53.76、F=7.74、F=54.49、F=16.94,균P＜ 0.05)；50 ～ 5000 nmol/L Bor처리세포24、48 h,bel-2단백표체축점하강,Bax단백표체축점증가.결론 Bor대노년백혈병환자원대세포구유억제증식、유도조망작용,기작용궤제가능여bcl-2가족단백적표체수평변화상관.
Objective To study the anti-tumor effect and mechanism of bortezomib in primary acute leukemia cells from elderly patients.Methods Primary acute leukemia cells were treated with bortezomib 50-5000 nmol/L for 24-48 h,cell proliferation was analysed by MTT assay; apoptosis of primary acute leukemia cells was observed by fluorescence microscopy and flow cytometry; protein expression of bcl-2 and Bax was detected by Western blot.Results The cell viability was 90 ％ and 70 ％ when leukemia cells were treated with 50 and 5000 nmol/L bortezomib for 24 h,respectively.Meanwhile,cells showed (10.2±2.3) ％ and (13.3±3.3) ％ apoptosis.With prolonged treatment for 48 h,cell viability decreased to 86 ％ and 60 ％,respectively,while the apoptosis rates were increased to(18.4±3.9) ％ and(20.7±3.7) ％.Compared to the control group 0 nmol/L bortezomib,the differences were statistically significant (F =53.76,F =7.74,F =54.49,F =16.94,all P values ＜ 0.05).With the increase of bortezomib concentration,the bcl-2 protein expression was decreased,while Bax was up-regulated.Conclusion Bortezomib can inhibit primary leukemia cells from elderly patients proliferation and induce apoptosis.The mechanism may be associated with the changes in bcl-2 family protein expression.
