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高瑞兰,金锦梅,牛泱平,谢桂丽,王文涛,马逢顺.人参总皂甙增加白血病细胞对化疗药物的敏感性[J].中国中西医结合杂志,1999,(1):17-19
人参总皂甙增加白血病细胞对化疗药物的敏感性
Potentiated Effects of Total Saponins of Panax Ginseng on Inhibition of Leukemic Cells by Cytotoxic Drugs
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DOI:
中文关键词:  人参总皂甙  白血病祖细胞集落形成  药敏试验
英文关键词:total saponins of Panax Ginseng  colony forming unite acute myeloid leukemia  drug sensitivity test
基金项目:浙江省自然科学基金
作者单位
高瑞兰 浙江中医学院附属医院 
金锦梅 浙江中医学院附属医院 
牛泱平 浙江中医学院附属医院 
谢桂丽 浙江中医学院附属医院 
王文涛 浙江中医学院附属医院 
马逢顺 浙江中医学院附属医院 
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中文摘要:
      目的:探讨人参总皂甙(TSPG)对急性髓细胞白血病(AML)化疗药物敏感性的作用。方法:采用白血病祖细胞集落形成(CFU AML)药敏试验法。选用4种化疗药物:高三尖杉酯碱(HHr)、阿糖胞苷(Ara)、阿霉素(Adr)和足叶乙甙(Vp 16)。结果:TSPG刺激CFU AML在体外增殖,集落数提高3798%,使化疗药物对CFU AML的抑制率从原先的304%~474%分别提高到512%~620%,增强了化疗药物对白血病祖细胞的杀伤作用,是无STPG的184~223倍。本研究72项药敏试验(4种化疗药物×18例)中有17项经TSPG的作用后由原先的不敏感转为敏感。结论:TSPG可使常规的化疗药物对白血病细胞的抑制作用增强。
英文摘要:
      Objective: To investigate the potentiated effects of total saponins of Panax Ginseng (TSPG) on inhibition of leukemic progenitor cells by cytotoxic drugs in acute myelocytic leukemia. Methods: Using bone marrow culture of colony forming unite acute myeloid leukemia (CFU AML) method, the sensitivity of leukemic cells obtained from 18 patients to homoharringtonin (HHr), cytarabine (Ara), adriamycin (Adr) and etoposide (VP 16) were detected separately. Results: TSPG alone (20μg/ml) could stimulate proliferation of CFU AML obviously, and increase the colony numbers by 37.98% over the non TSPG control (P<0 01). In the presence of TSPG, the inhibition rates of CFU AML of HHr, Ara, Adr and VP 16 were 51 2%~62 0% respectively, which were significantly higher than 30.4%~47.4% of non TSPG control (all P<0 01). In the combination of TSPG with cytotoxic drugs, the leukemic progenitor cells became more sensitive to cytotoxic drugs, CFU AML colony numbers at 1.84~2 23 fold as more as those of non TSPG control were inhibited by HHr, Ara, Adr and VP 16. Sensitivity test of 17 among 72 drugs reversed from resistant (suppression rate less than 30%) to sensitive (suppression rate more than 30%) by TSPG. Conclusions: TSPG could drive non cycling leukemic progenitors to enter cell cycle, and thereby enhance their susceptibility to cytotoxic drugs.
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