Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model

Xinyi Mu; Yanyan Zhang; Jing Li; Jieyu Xia; Xiongbin Chen; Pengwei Jing; Xiaoying Song; Lu Wang; Yaping Wang

doi:10.1155/2017/3508907

Angelica Sinensis Polysaccharide Prevents Hematopoietic Stem Cells Senescence in D-Galactose-Induced Aging Mouse Model

Stem Cells Int. 2017:2017:3508907. doi: 10.1155/2017/3508907. Epub 2017 Apr 11.

Authors

Xinyi Mu^{1

2}, Yanyan Zhang¹, Jing Li^{1

3}, Jieyu Xia^{1

2}, Xiongbin Chen^{1

2}, Pengwei Jing^{1

2}, Xiaoying Song^{1

2}, Lu Wang^{1

2}, Yaping Wang^{1

2}

Affiliations

¹ Laboratory of Stem Cells and Tissue Engineering, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China.
² Department of Histology and Embryology, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China.
³ Department of Pathophysiology, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China.

Abstract

Age-related regression in hematopoietic stem/progenitor cells (HSC/HPCs) limits replenishment of the blood and immune system and hence contributes to hematopoietic diseases and declined immunity. In this study, we employed D-gal-induced aging mouse model and observed the antiaging effects of Angelica Sinensis Polysaccharide (ASP), a major active ingredient in dong quai (Chinese Angelica Sinensis), on the Sca-1⁺ HSC/HPCs in vivo. ASP treatment prevents HSC/HPCs senescence with decreased AGEs levels in the serum, reduced SA-β-Gal positive cells, and promoted CFU-Mix formation in the D-gal administrated mouse. We further found that multiple mechanisms were involved: (1) ASP treatment prevented oxidative damage as total antioxidant capacity was increased and levels of reactive oxygen species (ROS), 8-OHdG, and 4-HNE were declined, (2) ASP reduced the expression of γ-H2A.X which is a DNA double strand breaks (DSBs) marker and decreased the subsequent ectopic expressions of effectors in p16^Ink4a-RB and p19^Arf-p21^Cip1/Waf senescent pathways, and (3) ASP inhibited the excessive activation of Wnt/β-catenin signaling in aged HSC/HPCs, as the expressions of β-catenin, phospho-GSK-3β, and TCF-4 were decreased, and the cyto-nuclear translocation of β-catenin was inhibited. Moreover, compared with the positive control of Vitamin E, ASP exhibited a better antiaging effect and a weaker antioxidation ability, suggesting a novel protective role of ASP in the hematopoietic system.