As2O3下调KG1a细胞粘附分子CD44、CD49d表达

目的探讨三氧化二砷（As2O3）对体外造血微环境中KG1a细胞粘附分子CD44和CD49d表达的影响。方法用正常人和白血病患者的骨髓基质细胞在体外模拟造血微环境,与KG1a细胞共培养。用流式细胞术检测不同条件下As2O3对KG1a细胞CD44和CD49d表达的影响。结果来源于正常人或白血病患者的骨髓基质细胞与KG1a细胞共培养都可明显增加KG1a细胞CD44、CD49d表达（P≤0.01）,但两种不同来源的骨髓基质细胞上调KG1a细胞CD44、CD49d表达无明显差异（P〉0.05）;骨髓基质细胞与KG1a细胞共培养的时间对CD44和CD49d表达无影响（P〉0.05）。在共培养体中,不同浓度As2O3均可下调KG1a细胞CD44、CD49d的表达。用1μmol/L的As2O3分别作用24h及48 h后,KG1a细胞表面CD44分别为（94.32±0.77）%和（88.97±1.74）%（P〈0.05）;CD49d分别为（41.12±0.37）%和（34.12±1.77）%（P〈0.05）,随时间延长表达下降。当As2O3浓度增高为2μmol/L时,CD44表达率由（99.08±0.29）%降至（85.6±0.88）%,CD49d表达率由（47.48±0.1）%降至（37.03±0.96）%（P〈0.01）。结论 As2O3能降低体外造血微环境中KG1a细胞表面CD44、CD49d表达,并且呈时间剂量依赖性。

Down-regulation of CD44 and CD49d expression of KG1a cells by arsenic trioxide

Objective To explore the effect of arsenic trioxide（As2O3） on adhesion molecules of leukemia cells in hematopoietic microenvironment.Methods BMSCs were isolated by whole bone marrow culture method,and co-cultured with human acute myeloid leukemic cell line KG1a cells in vitro.After treatment with As2O3,inhibition rate of suspended KG1a cells detected by MTT,and calculated IC50 values of As2O3 by SPSS probit analysis.The expression of CD44 and CD49d of KG1a were analyzed by flow cytometry.Results The expression of CD44 and CD49d of BMSCs co-cultured KG1a cells were significantly higher than KG1a cells without co-culture（P≤0.01）,but the difference between KG1a cells co-cultured with normal and leukemic BMSCs was not significant（P0.05）.The co-culture time of 24 hours and 48 hours with BMSCs and KGIa did not affect the expression of CD44 and CD49d（P0.05）.In leukemic BMSCs co-cultured system,the expression of CD44 decreased from 99.08±0.29% to 85.6±0.88%,CD49d decreased from 47.48±0.1% to 37.03±0.96% by the treatment with 2μmol/L As2O3（P0.01 respectively）;When treated with 1 μmol/L As2O3 for different length of time,the expression of CD44 and CD49d of leukemic BMSCs-cocultured KG1a cells were decreased（P0.05）.Conclusion Arsenic trioxide may reduce the expression of CD44 and CD49d of KG1a cell in vitro hematopoietic microenvironment.