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作 者:周亚丽[1] 彭志刚[2] 张晓梅[2] 罗军[2] 赖永榕[2]
机构地区:[1]解放军303医院血液科,南宁530021 [2]广西医科大学第一附属医院血液科
出 处:《临床血液学杂志》2010年第2期104-106,共3页Journal of Clinical Hematology
摘 要:目的:研究氟达拉滨在体外对多发性骨髓瘤细胞系KM3细胞的生长抑制、诱导凋亡作用及对细胞自分泌细胞因子的影响。方法:采用MTT法观察不同浓度氟达拉滨对KM3细胞生长的影响;用AnnexinⅤ/PI双染法流式细胞仪检测KM3的凋亡率;用双抗夹心法(ELISA)检测上清液中VEGF、IL-6和可溶性IL-6受体(sIL-6R)的水平。结果:①氟达拉滨对KM3细胞有明显的抑制作用,并随药物浓度升高和作用时间的延长而抑制作用增强。MTT法显示,氟达拉滨作用于KM3细胞72h后,其半数抑制率IC50约为95nmol/L。25~400nmol/L浓度范围氟达拉滨作用72h后,KM3细胞的凋亡率随药物浓度的增加而升高。②KM3细胞经氟达拉滨作用72h后,上清液中VEGF和sIL-6R水平随药物浓度的升高逐渐下降,而IL-6水平先升高后明显下降。结论:氟达拉滨能明显抑制KM3细胞的增殖并诱导其细胞凋亡,同时能抑制KM3细胞自分泌VEGF、IL-6和sIL-6R。Objective:To study the effects of fludarabine on growth of multiple myeloma KM3 cells and the influence of fludarabine on autocrining level of cytokines.Method:The effects of different concentrations of fludarabine on the proliferation of KM3 multiple myeloma cells were examined by MTT assay. The apoptosis of KM3 cells was stained with AnnexinⅤ/PI and detected by flow cytometr. The levels of IL-6 and sIL-6R autosecreted by KM3 cells were tested by ELISA after KM3 cells were treated with fludarabine. Result:Fludarabine inhibited the proliferation of KM3 cells and the inhibition effect were dependent on time and concentration.The MTT assay showed that the IC50 was 95 nmol/L with fludarabine treatment for 72 hours. The apoptosis rate of KM3 cells increased with fludarabine treatment at a dosage within 25400 nmol/L. Fludarabine decreased the autocrining level of IL-6 slightly,and inhibited the level of VEGF and sIL-6R obviously. Conclusion:The proliferation of KM3 cells was markedly inhibited by fludarabine in a dose-dependent and time-dependent manner. Fludarabine can also decrease the level of VEGF,IL-6 and sIL-6R autocrined by KM3 cells.
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