摘要
本研究通过观察抑制SDF 1活性对HL 6 0细胞增殖活性的影响 ,探讨趋化因子SDF 1在维持HL 6 0细胞生存能力中的作用。培养骨髓基质细胞 ,并与HL 6 0细胞共培养 ,采用SDF 1受体CXCR4单克隆抗体阻断SDF 1生物活性后 ,用MTT法检测HL 6 0细胞活力、用流式细胞术观察HL 6 0细胞增殖周期变化、检测细胞膜表面CXCR4表达 ,同时检测CXCR4单克隆抗体应用前后HL 6 0细胞内钙离子浓度变化。结果显示 ,抗CXCR4单克隆抗体可下调HL 6 0细胞膜表面CXCR4的表达 ,同时处于G0 /G1期的细胞增多 ,处于S期的细胞减少 ,而白血病细胞存活率下调 ,细胞内钙离子浓度降低。结论 :抑制SDF
This study was aimed to investigate the importance of chemokine SDF 1 in maintaining proliferation ability of acute myelocytic leukemia cell line HL 60 when the effects of SDF 1 on HL 60 cell proliferation were inhibeted. Marrow stromal cells were cultured and co cultured with HL 60 cells, and SDF 1 activity was blocked with anti CXCR4 McAb. HL 60 cell activity was detected by MTT while cell cycle and the expression of CXCR4 on HL 60 cell membrane were observed by flow cytometry meanwhile. The internal calcium ionic concentration in HL 60 cell was detected as well before and after treated with 12G5. The results showed that 12G5 down regulated the expression of CXCR4 on HL 60 cell membrane; HL 60 cells at G 0/G 1 phase increased,but decreased at S phase; survive rate of leukemia cells reduced; the intercellular calcium ionic concentration of HL 60 cell decreased after treated with 12G5. It was concluded that brockage of the SDF 1 activity may inhibit proliferation of leukemia cell at certain level.
出处
《中国实验血液学杂志》
CAS
CSCD
2004年第2期154-158,共5页
Journal of Experimental Hematology
基金
国家自然科学基金项目资助项目
编号3 0 170 3 96