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粒细胞集落刺激因子影响阿糖胞苷诱导HL-60白血病细胞凋亡的研究
引用本文:林东军,黄仁魏,范珺,王东宁,付咏梅. 粒细胞集落刺激因子影响阿糖胞苷诱导HL-60白血病细胞凋亡的研究[J]. 中国病理生理杂志, 2000, 16(11): 1207-1209
作者姓名:林东军  黄仁魏  范珺  王东宁  付咏梅
作者单位:1. 中山医科大学附属第三医院血液肿瘤科, 广东 广州510630;
2. 暨南大学医学院病理生理教研室, 广东 广州 510632
摘    要:目的:观察粒细胞集落刺激因子(G-CSF)对阿糖胞苷(Ara-C)诱导HL-60白血病细胞凋亡的调控作用。方法:应用细胞培养技术、细胞凋亡形态、二苯胺法DNA片段化定量和MTT法来观察HL-60白血病细胞的增殖、凋亡和细胞药敏的变化。结果:G-CSF有刺激HL-60白血病细胞的增殖的作用,其细胞集落为76.5±18.0,而对照组仅为46.5±13.5(P<0.01,n=5)。Ara-C(10 mg/L)作用于HL-60白血病细胞4 h,DNA片段率为32.3%±6.5%,同时加入G-CSF和Ara-C作用于HL-60白血病细胞4 h;DNA片段率为23.6%±7.2%,两组比较有非常显著性差异(P<0.01)。HL-60白血病细胞加入G-CSF后对Ara-C的IC50(18.85±3.21)可看出比单用Ara-C(15.29±2.47)的敏感性低(P<0.05)。结论:G-CSF能刺激HL-60白血病细胞增殖;抑制Ara-C诱导HL-60白血病细胞的凋亡;能降低HL-60白血病细胞对Ara-C的敏感性。

关 键 词:细胞系  白血病  凋亡  阿糖胞苷  粒细胞集落刺激因子  
文章编号:1000-4718(2000)11-1207-03
收稿时间:2000-09-28
修稿时间:2000-09-28

Effect of G-CSF on the apoptosis induced by Ara-c in HL-60 leukemic cells
LIN Dong-jun,HUANG Ren-wei,FAN Jun,WANG Dong-ning,FU Yong-mei. Effect of G-CSF on the apoptosis induced by Ara-c in HL-60 leukemic cells[J]. Chinese Journal of Pathophysiology, 2000, 16(11): 1207-1209
Authors:LIN Dong-jun  HUANG Ren-wei  FAN Jun  WANG Dong-ning  FU Yong-mei
Affiliation:1. Department of Hematology, Sun Yat-sen University of Medical Sciences, Guangzhou 510630, China;
2. Department of Pathophysiology, Medical College of Jinan University, Guangzhou 510632, China
Abstract:AIM: To observe the effects of methionine-induced hyperhomocysteinemia on protein C(PC), antithrombin-Ⅲ (AT-Ⅲ) and von willebrand factor (vWF).METHODS:The proliferat ion of HL-60 leukemia cell was observed by hemopoiet ic cell culture.Apoptosis was measured by the morphology of apoptosis cell, the quantitation of DNA fragmentation with the diphenylamine reaction.The change in drug sensitivity was measured by MTT.RESULTS:In group M, the levels of methionine(29.97±5.34 μmol/L) and homocysteine(13.30±2.19 μmol/L) in serum were signifficantly higher than those(14.48±1.97 μmol/L and 5.36±1.19 μmol/L, respectively, P<0.01) of group C.The levels of AT-Ⅲ and PC of group M were signifficantly lower than those of group C (P<0.01). The level of vWF in plasma of group M was higher than that of group C (P<0.01). Immunohistochemistry showed that vWF expression in endothelial cells of aorta was decreased. CONCLUSION:Methionine-induced hyperhomocysteinemia had promotive effects on coagulation and inhibiting effects on antioagulation.
Keywords:Cell line   Leukemia   Apoptosis   Cytarabine  Granulocyte colony-stimulating factor
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