Zhang Xian-Ping, Liu Jun, Xu Chun-Yan, Wei Qiang, Li Jing, Wang Lu, Wang Jian-Wei, Wang Ya-Ping
Department of Histology and Embryology, Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing 400016, China.
Zhongguo Zhong Yao Za Zhi. 2013 Jul;38(14):2354-8.
To observe the effect of Angelica sinensis polysaccharides (ASP) on the length of telomere, the activity of telomerase and the expression of P53 protein in mice hematopoietic stem cells (HSCs), and explore ASP's potential mechanism for regulating HSC aging.
C57BL/6J mice were randomly divided into the normal group, the aging group and the intervention group. The aging group was radiated with X ray to establish the mice aging HSC model. The intervention group was orally administered with ASP during X-ray irradiation, while the normal group was orally administered with NS. Their HSCs were isolated by immunomagnetic beads. Cell cycles analysis and senescence-associated beta-galactosidase (SA-beta-Gal) staining were used to detect changes in aging HSCs. The expression of P53 was determined by western blot analysis. The length of telomere and the vitality of telomerase were analyzed by southern blot and TRAP-PCR, respectively.
Compared with the normal group, X-ray irradiation could significantly increase the cell ratio of in HSC G1 stage, rate of SA-beta-Gal positive cells and expression of P53 protein, and reduce the length of telomere and the vitality of telomerase. Compared with the aging group, ASP could significantly inhibit the cell ratio of in HSC G1 stage and the increase in the number of SA-beta-Gal positive cells, down-regulate the expression of P53 protein, and increase the length of telomere and the vitality of telomerase in HSCs.
ASP could antagonize X-ray-induced aging of HSCs, which may be related to the increase in the length of telomere and the activity of telomerase, as well as the down-regulation of the expression of P53 protein.
观察当归多糖（ASP）对小鼠造血干细胞（HSCs）端粒长度、端粒酶活性及P53蛋白表达的影响，探讨ASP调控HSC衰老的潜在机制。
将C57BL/6J小鼠随机分为正常组、衰老组和干预组。衰老组采用X射线照射建立小鼠衰老HSC模型。干预组在X射线照射期间口服ASP，正常组口服生理盐水。通过免疫磁珠分离其HSCs。采用细胞周期分析和衰老相关β-半乳糖苷酶（SA-β-Gal）染色检测衰老HSCs的变化。通过蛋白质免疫印迹分析测定P53的表达。分别采用Southern印迹法和TRAP-PCR法分析端粒长度和端粒酶活性。
与正常组相比，X射线照射可显著增加HSC G1期细胞比例、SA-β-Gal阳性细胞率及P53蛋白表达，缩短端粒长度，降低端粒酶活性。与衰老组相比，ASP可显著抑制HSC G1期细胞比例及SA-β-Gal阳性细胞数量的增加，下调P53蛋白表达，增加HSCs中端粒长度和端粒酶活性。
ASP可拮抗X射线诱导的HSCs衰老，这可能与端粒长度增加、端粒酶活性增强以及P53蛋白表达下调有关。
