白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2013年
9期
535-537
,共3页
张亚停%方建培%翁文骏%许吕宏%庄豪
張亞停%方建培%翁文駿%許呂宏%莊豪
장아정%방건배%옹문준%허려굉%장호
骨髓基质细胞%白血病%抗晚期抗原4抗体%细胞增殖%凋亡
骨髓基質細胞%白血病%抗晚期抗原4抗體%細胞增殖%凋亡
골수기질세포%백혈병%항만기항원4항체%세포증식%조망
Bone marrow stromal cells%Leukemia%Antibody against late antigen-4%Cell proliferation%Apoptosis
目的 探讨骨髓基质细胞、抗晚期抗原4抗体(aVLA-4)、阿糖胞苷(Ara-C)对白血病HL-60细胞增殖和凋亡的影响.方法 实验共分为5组:HL-60细胞单独培养组(对照组),HL-60细胞+基质细胞组(基质细胞组),HL-60细胞+基质细胞+aVLA-4组(抗体组),HL-60细胞+基质细胞+Ara-C组(药物组),HL-60细胞+基质细胞+aVLA-4+Ara-C组(抗体+药物组).采用CCK-8法检测各组细胞增殖或抑制率,流式细胞术检测各组HL-60细胞凋亡情况,Western blot法检测各组HL-60细胞中抗凋亡基因bc1-2表达情况.结果 基质细胞组培养24 h及48 h后HL-60细胞数量均高于对照组,差异有统计学意义[(7.2±0.3) ×105/ml比(5.3±0.4)×105/ml,(8.4±0.2)×105/ml比(6.8±0.3)×105/ml(P<0.001)];与基质细胞组比较,抗体组、药物组、抗体+药物组HL-60白血病细胞的增殖抑制率[(24.3±2.1)%、(37.0±2.6)%、(65.6±3.8)%]及凋亡率[(5.7±0.6)%、(8.0±0.5)%、(10.4±0.9)%、(16.5±0.7)%]均增高,差异有统计学意义(P<0.05),并以抗体+药物组的增高最为明显;各组的bcl-2蛋白表达均有下降,以抗体+药物组的下降最明显.结论 骨髓基质细胞对白血病细胞的增殖起促进作用,aVLA-4干扰基质细胞与白血病细胞间的相互作用可增强白血病细胞对Ara-C的化疗敏感性.
目的 探討骨髓基質細胞、抗晚期抗原4抗體(aVLA-4)、阿糖胞苷(Ara-C)對白血病HL-60細胞增殖和凋亡的影響.方法 實驗共分為5組:HL-60細胞單獨培養組(對照組),HL-60細胞+基質細胞組(基質細胞組),HL-60細胞+基質細胞+aVLA-4組(抗體組),HL-60細胞+基質細胞+Ara-C組(藥物組),HL-60細胞+基質細胞+aVLA-4+Ara-C組(抗體+藥物組).採用CCK-8法檢測各組細胞增殖或抑製率,流式細胞術檢測各組HL-60細胞凋亡情況,Western blot法檢測各組HL-60細胞中抗凋亡基因bc1-2錶達情況.結果 基質細胞組培養24 h及48 h後HL-60細胞數量均高于對照組,差異有統計學意義[(7.2±0.3) ×105/ml比(5.3±0.4)×105/ml,(8.4±0.2)×105/ml比(6.8±0.3)×105/ml(P<0.001)];與基質細胞組比較,抗體組、藥物組、抗體+藥物組HL-60白血病細胞的增殖抑製率[(24.3±2.1)%、(37.0±2.6)%、(65.6±3.8)%]及凋亡率[(5.7±0.6)%、(8.0±0.5)%、(10.4±0.9)%、(16.5±0.7)%]均增高,差異有統計學意義(P<0.05),併以抗體+藥物組的增高最為明顯;各組的bcl-2蛋白錶達均有下降,以抗體+藥物組的下降最明顯.結論 骨髓基質細胞對白血病細胞的增殖起促進作用,aVLA-4榦擾基質細胞與白血病細胞間的相互作用可增彊白血病細胞對Ara-C的化療敏感性.
목적 탐토골수기질세포、항만기항원4항체(aVLA-4)、아당포감(Ara-C)대백혈병HL-60세포증식화조망적영향.방법 실험공분위5조:HL-60세포단독배양조(대조조),HL-60세포+기질세포조(기질세포조),HL-60세포+기질세포+aVLA-4조(항체조),HL-60세포+기질세포+Ara-C조(약물조),HL-60세포+기질세포+aVLA-4+Ara-C조(항체+약물조).채용CCK-8법검측각조세포증식혹억제솔,류식세포술검측각조HL-60세포조망정황,Western blot법검측각조HL-60세포중항조망기인bc1-2표체정황.결과 기질세포조배양24 h급48 h후HL-60세포수량균고우대조조,차이유통계학의의[(7.2±0.3) ×105/ml비(5.3±0.4)×105/ml,(8.4±0.2)×105/ml비(6.8±0.3)×105/ml(P<0.001)];여기질세포조비교,항체조、약물조、항체+약물조HL-60백혈병세포적증식억제솔[(24.3±2.1)%、(37.0±2.6)%、(65.6±3.8)%]급조망솔[(5.7±0.6)%、(8.0±0.5)%、(10.4±0.9)%、(16.5±0.7)%]균증고,차이유통계학의의(P<0.05),병이항체+약물조적증고최위명현;각조적bcl-2단백표체균유하강,이항체+약물조적하강최명현.결론 골수기질세포대백혈병세포적증식기촉진작용,aVLA-4간우기질세포여백혈병세포간적상호작용가증강백혈병세포대Ara-C적화료민감성.
Objective To explore the bone marrow stromal cells,anti-late antigen-4 (VLA-4) antibody (aVLA-4),cytarabine (Ara-C) on the proliferation and apoptosis of leukemia HL-60 cells.Methods The experiment was divided into five groups:HL-60 cells were cultured alone (control group),HL-60 cells and stromal cells group (stromal cells group),HL-60 cells + stromal cells + aVLA-4 (antibody group),HL-60 cells + stromal cells + Ara-C group (drug group),HL-60 cells + stromal cells + aVLA-4 + Ara-C group (antibody +drug group).Cell proliferation or inhibition rate was detected by CCK-8 method,the HL-60 cells apoptosis was detected by flow cytometry.The expression of anti-apoptotic gene bcl-2 in HL-60 cells was determined by Western blot.Results After 24 h and 48 h,treatment,the number of the stromal cells group HL-60 cells were higher than that of the control group with significant difference cultured [(7.2±0.3)×1O5/ml vs (5.3±0.4)×105/ml,(8.4±0.2)×105/ml vs (6.8±0.3)×105/m1,P < 0.001],while the HL-60 cell proliferation inhibition rate [(24.3±2.1) %,(37.0±2.6) %,(65.6±3.8) %] and apoptosis rate [(5.7±0.6) %,(8.0±0.5) %,(10.4±0.9) %,(16.5±0.7) %] of antibody group,drug group,antibody + drug group were higher than the control group with a difference of statistically significant (P < 0.05),and the increase of antibody + drug group was most obvious.With the decreasing of the bcl-2 protein expression,which was most the decrease of antibody + drug group was most obvious.Conclusion Bone marrow stromal cells can stimulate the proliferation of leukemia cells,aVLA-4 interference the interaction between stromal cells and leukemia cells can enhance the chemosensitivity of leukemia cells to Ara-C.