中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (49): 9225-.doi: 10.3969/j.issn.1673-8225.2010.49.024

• 干细胞与中医药 • 上一篇    下一篇

人参多糖注射液体外诱导人白血病细胞株K562增殖抑制及分化

何 轩1，姜蓉1，李静1，左国伟2，雷翠蓉1，王亚平1，王建伟1，陈地龙1   

  1. 1重庆医科大学组织胚胎教研室，干细胞与组织工程研究室，重庆市   400016；2重庆医科大学临床检验诊断学省部共建教育部重点实验室，重庆市
    400016
  • 出版日期:2010-12-03 发布日期:2010-12-03
  • 通讯作者: 陈地龙，重庆医科大学组织胚胎教研室，干细胞与组织工程研究室，重庆市 400016 chendilong@21cn.com
  • 作者简介:何轩★，男，1981年生，重庆市綦江县人，汉族，2004年重庆医科大学毕业，重庆医科大学在读硕士，助教，主要从事人体解剖与组织胚胎研究。 c2109@163.com
  • 基金资助:

    国家自然科学基金面上项目，编号：30873406，课题名称：人参多糖对人白血病K562细胞株增殖抑制作用及诱导分化的分子靶点研究。

Proliferative inhibition and differentiation of leukemia K562 cells induced by ginseng polysaccharide in vitro

He Xuan1, Jiang Rong1, Li Jing1, Zuo Guo-wei2, Lei Cui-rong1, Wang Ya-ping1, Wang Jian-wei1, Chen Di-long1   

  1. 1Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing  400016, China; 2Province-Ministry Co-construction Key Laboratory of Clinical Inspection and Diagnostics, Ministry of Education, Chongqing Medical University, Chongqing  400016, China
  • Online:2010-12-03 Published:2010-12-03
  • Contact: Chen Di-long, Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing 400016, China chendilong@21cn.com
  • About author:He Xuan★, Studying for master’s degree, Assistant, Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing 400016, China c2109@163.com
  • Supported by:

     the General Program of  National Natural Science Foundation of China, No: 30873406*

PDF

475

被引次数

17

摘要：

背景：既往研究表明，人参多糖既能促进正常血细胞生成，又能抑制白血病细胞的增殖，但这种双向调控的机制尚不清楚。
目的：体外观察人参多糖注射液对人白血病细胞株K562增殖抑制及诱导分化的影响。
方法：K562细胞由重庆医科大学临床检验系提供，人参多糖注射液为山西普德药业有限公司生产。取对数生长期的K562细胞，调整浓度为7×108 L-1。对照组予以常规培养；人参多糖组分别加入25，50，100，200，400，600，800 mg/L的人参多糖注射液。MTT比色法检测人参多糖注射液对K562细胞增殖情况的影响；血红蛋白测定及联苯胺、Wright’s染色检测K562细胞向红系细胞分化的特征；流式细胞仪测定细胞凋亡情况。
结果与结论：人参多糖在体外对 K562细胞的增殖有明显抑制作用，并能诱导K562细胞向红系细胞分化，表现为K562细胞的增殖受到抑制。K562细胞形态学上可见细胞体积缩小，核直径减小，胞浆丰富，核浆比例降低；人参多糖在体外对K562细胞有诱导血红蛋白生成的作用，在100~800 mg/L范围内，呈浓度依赖性，且均在作用48 h时抑制率达高峰；细胞凋亡率增加。提示人参多糖注射液能抑制K562细胞增殖，诱导其凋亡，并使K562细胞向红系细胞方向分化。

关键词: 人参多糖注射液, K562细胞, 增殖抑制, 诱导分化, 细胞凋亡

Abstract:

BACKGROUND: Ginseng polysaccharide can promote normal hematopoiesis and inhibit proliferation of leukemia K562 cells. However, their mechanisms have not been known.
OBJECTIVE: To investigate the effect of ginseng polysaccharide on proliferation and differentiation of chronic myelocytic leukemia K562 cells in vitro.
METHODS: K562 cells were kindly presented by Department of Clinical Laboratory, Chongqing Medical University. Ginseng polysaccharide was purchased from Shanxi Pude Medicines Co., Ltd. The density of K562 cells with logarithmic phase was regulated to 7×108/L. The conventional culture was performed in the blank control group. Ginseng polysaccharide group was incubated with 25, 50, 100, 200, 400, 600, 800 mg/L ginseng polysaccharide respectively. The proliferation of K562 cells was examined by MTT; Benzidine and Wright’s staining were used to observe the features of erythroid lineage differentiated from K562 cells. Meantime, the apoptotic rate of K562 cells was determined by flow cytometry.
RESULTS AND CONCLUSION: Ginseng polysaccharide could significantly inhibit the proliferation and promote differentiation of K562 cells into erythroid linage cells in vitro. The proliferation of K562 cells was inhibited. The morphological feature of K562 cells tended to be more mature, showing small volume, reduced nuclear diameter, abundant cytoplasm, and decreased karyoplasmic ratio. Hemoglobin in K562 cells induced by ginseng polysaccharide increased significantly. Apoptotic rate of K562 cells treated with ginseng polysaccharide (100-800 mg/L) increased significantly in a concentration dependent fashion; the inhibitory rate reached a peak at 48 hours. These indicate that ginseng polysaccharide may inhibit the proliferation of K562 cells, promote their apoptosis and induce the differentiation of K562 cells into erythroid cells.

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