中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (23): 4272-4276.doi: 10.3969/j.issn.1673-8225.2011.23.021

• 干细胞与中医药 stem cells and traditional Chinese medicine • 上一篇    下一篇

黄芪多糖对2型糖尿病患者外周血内皮祖细胞PI3K/Akt/eNOS信号通路的影响

徐寒松1，吴  青1，谢晓云2，孔德明1   

  1. 1贵阳中医学院第二附属医院内分泌科，贵州省贵阳市  550003
    2中南大学湘雅三医院，湖南省长沙市   410000
  • 收稿日期:2011-03-15 修回日期:2011-04-13 出版日期:2011-06-04 发布日期:2011-06-04
  • 作者简介:徐寒松☆，男，1973年生，贵州省安顺市人，汉族，2007年中南大学湘雅医院毕业，博士，副教授，内分泌科主任，硕士生导师，主要从事糖尿病慢性并发症的研究。 xuhansong911@163.com 并列第一作者：吴　青★，女，1984年生，湖南省新化县人，贵阳中医学院在读硕士，主要从事糖尿病慢性并发症的研究。 269426020@qq.com
  • 基金资助:

    国家自然科学基金资助项目(30960491)；贵州省优秀科技教育人才省长基金资助项目[黔省专合字(2009)84号]。

Effect of astragalus polysaccharides on peripheral endothelial progenitor cells via PI3K/Akt/eNOS signal pathway in patients with type 2 diabetes  

Xu Han-song1, Wu Qing1, Xie Xiao-yun2, Kong De-ming1   

  1. 1Department of Endocrinology, the Second Affiliated Hospital of Guiyang College of Traditional Chinese Medicine, Guiyang  550003, Guizhou Province, China
    2Xiangya Third Hospital of Central South University, Changsha  410000, Hunan Province, China
  • Received:2011-03-15 Revised:2011-04-13 Online:2011-06-04 Published:2011-06-04
  • About author:Xu Han-song☆, Doctor, Associate professor, Master’s supervisor, Department of Endocrinology, the Second Affiliated Hospital of Guiyang College of Traditional Chinese Medicine, Guiyang 550003, Guizhou Province, China xuhansong911@163.com Wu Qing, Studying for master’s degree, Department of Endocrinology, the Second Affiliated Hospital of Guiyang College of Traditional Chinese Medicine, Guiyang 550003, Guizhou Province, China 269426020@qq.com Xu Han-song and Wu Qing contributed equally to this paper.
  • Supported by:

    the National Natural Science Foundation of China, No. 30960491*; Guizhou Provincial Governor Funding for the Outstanding Education Professionals, No. (2009)84*

PDF

393

被引次数

53

摘要：

背景：前期研究证实黄芪通过P38MAPK通路促进内皮祖细胞增殖，其影响是否通过PI3K/Akt/eNOS途径实现？
目的：观察黄芪多糖对2型糖尿病患者外周血内皮祖细胞蛋白激酶B、内皮型一氧化氮合酶表达的影响。
方法：采用密度梯度离心法获取糖尿病患者外周血单个核细胞，培养7 d后鉴定内皮祖细胞。观察0，50，200，800，3 200，6 400 mg/L黄芪多糖分别干预6，12，24，48 h对内皮祖细胞影响的量效和时效关系；用黄芪多糖及黄芪多糖与PI3K抑制剂LY294002联合干预糖尿病患者内皮祖细胞，Western blot检测磷酸化Akt及磷酸化内皮型一氧化氮合酶的表达水平。以未进行任何处理健康人内皮祖细胞作为对照组。
结果与结论：糖尿病患者内皮祖细胞的增殖能力较对照组明显下降(P  < 0.05)。黄芪多糖显著增加糖尿病患者内皮祖细胞的增殖能力，当黄芪多糖在200~800 mg/L质量浓度范围，干预6~24 h可呈时间及剂量依赖性增强内皮祖细胞的增殖能力(P < 0.01)，并呈剂量依赖性升高内皮祖细胞磷酸化Akt及磷酸化内皮型一氧化氮合酶的表达(P < 0.05)；PI3K抑制剂LY294002能阻断黄芪多糖诱导的Akt、内皮型一氧化氮合酶的磷酸化(P < 0.05)。说明黄芪多糖通过激活PI3K/Akt/eNOS信号通路促进内皮祖细胞增殖和向内皮细胞的分化。

关键词: 黄芪多糖, 内皮祖细胞, 内皮型一氧化氮合酶, 磷脂酰肌醇-3激酶, 蛋白激酶B

Abstract:

BACKGROUND: Previous studies have demonstrated that Astragalus can promote the proliferation of endothelial progenitor cells (EPCs) via P38MAPK pathway. Whether PI3K/Akt/eNOS signal pathway can replace P38MAPK pathway needs further studies.
OBJECTIVE: To observe the effect of astragalus polysaccharides (APS) on the expression of protein kinase B (PKB) and endothelial nitric oxide synthase (eNOS) of EPCs from peripheral blood in patients with type 2 diabetes.
METHODS: Mononuclear cells from diabetic patients were isolated by Ficoll density gradient centrifugation, and identified as EPCs after 7 days. Dose-depended and time-depended effects of APS with six different concentrations (0, 50, 200, 800, 3 200,
6 400 mg/L) and different treatment time (6, 12, 24, 48 hours) on EPCs proliferation and differentiation were measured. EPCs were treated with APS alone or APS combined with LY294002 to observe the expressions phosphorylated Akt and eNOS using Western Blot. EPCs from healthy persons were used as controls.
RESULTS AND CONCLUSION: The proliferative ability of EPCs in the diabetic group was significantly lower than that in the control group (P < 0.05). 200-800 mg/L APS within 6-24 hours could promote the proliferative ability of EPCs in a time- and dose-depended manner (P< 0.01). With dose increasing, the expressions of phosphorylated Akt and eNOS were also increased (P < 0.05). LY294002 could inhibit the phosphorylation of Akt and eNOS (P < 0.05). The findings indicate that APS can promote the proliferation and differentiation of EPCs into endothelial cells via activated PI3K/Akt/eNOS pathway.

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