血府逐瘀汤影响慢性粒细胞白血病VEGF表达的体外研究

张还珠; 邝枣园; 谭获; 黄振倩

文章摘要

张还珠邝枣园谭获黄振倩.血府逐瘀汤影响慢性粒细胞白血病VEGF表达的体外研究[J].实用中西医结合临床,2007,(4):1-2

血府逐瘀汤影响慢性粒细胞白血病VEGF表达的体外研究

DOI：

中文关键词: 慢性髓细胞性白血病血府逐瘀汤血管内皮生长因子

英文关键词: chronic myeloid leukemia xue fu zhu yu tang vascular endothelial growth factor

基金项目:广东省中医药局课题（课题编号2040038）

作者	单位
张还珠邝枣园谭获黄振倩	广州医学院第一附属医院广州中医药大学

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中文摘要:

目的：体外研究血府逐瘀汤含药血清对慢性粒细胞白血病细胞VEGF表达的影响。方法：采用酶联免疫吸附法（ELISA）检测20例初治CML患者、20例正常人骨髓细胞以及人慢性粒红白血病急性变K562细胞上清液的VEGF含量，并测定CML原代细胞和K562细胞加入不同浓度血府逐瘀汤含药血清共同培养后上清液的VEGF含量。结果：CML原代细胞上清液VEGF浓度为（389.27±65.77）pg/mL、K562细胞VEGF浓度为（461.24±137.57）pg/mL，均比正常人（125.45 ±28.24）pg/mL显著增高（P < 0.05），加入不同浓度的含药血清，在中、高浓度范围，CML原代细胞、K562细胞VEGF表达均明显下降，分别为（152.43±26.29）pg/mL、（80.31±19.73）pg/mL和（188.86±32.77）pg/mL、（114.81±14.16）pg/mL（P <0.05）。结论：异常血管新生可能参与CML发病，血府逐瘀汤含药血清在体外能显著抑制CML原代细胞和K562白血病细胞表达VEGF，该方有参与抑制CML异常血管形成的作用。

英文摘要:

Objectives To study the role of XUE FU ZHU YU TANG on expression of vascular endothelial growth factor (VEGF )in K562 cell line. Methods: VEGF level was assessed by ELISA in the cultural supernatants of bone marrow mononuclear cells from 20 chronic myeloid leukemia (CML) patients and 20 normal persons, and also of K562 cells. CML cells and K562 cells were respectively treated with serum containing of XUE FU ZHU YU TANG in different concentrations, the VEGF level in the cultural supernatants of the cells was detected by the same way. Result: The supernatants of cultured bone marrow cells from 20 CML patients and K562 cells contained significantly higher VEGF levels (389.27±65.77）pg/mL,（461.24 ±137.57）pg/mL,respectively than that in 20 normal control samples(125.45±28.24）pg/mL(P <0.05).CML cells and K562 cells treated with serum containing of XUE FU ZHU YU TANG in different concentrations resulted in significant reduction of VEGF levels (152.43±26.29）pg/mL,（80.31±19.73）pg/mL and（188.86±32.77）pg/mL,（114.81±14.16）pg/mL, respectively(P <0.05).Conclusion:Abnormal angiogenesis might play a role in the pathogenesis of CML. The serum containing of XUE FU ZHU YU TANG suppresses significantly VEGF expression of K562 cells. It is probably an additional anticancer mechanism for XUE FU ZHU YU TANG to inhibit abnormal angiogenesis in CML.

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