Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (23): 4272-4276.doi: 10.3969/j.issn.1673-8225.2011.23.021

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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*

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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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