当归多糖对造血干细胞SIRT1、p53和p21表达的影响

目的 研究当归多糖（ASP）基于辐射所致小鼠衰老造血干细胞（HSCs） SIRT1、p53和p21蛋白表达的影响，探讨ASP基于调控HSCs衰老的可能机制。方法72只SPF级C57BL/6J小鼠随机纳入对照组、模型组和ASP组。模型组通过X线3.0G y/8F全身照射建立小鼠HSCs衰老模型；ASP组在照射期间给予ASP灌胃；对照组与模型组予生理盐水。经免疫磁珠法分选小鼠HSCs，采用流式细胞术检测细胞周期，通过β-半乳糖苷酶（SA-β-Gal）染色观察衰老细胞；经混合集落培养（CFU-Mix）观察HSCs自我更新及定向分化潜能；Western blot检测SIRT1、p53、p21蛋白表达。结果与对照组比较，X线照射可能显著增加模型组HSCs G1期细胞比例、SA-β-Gal染色阳性细胞率、p53及p21蛋白表达（P<0.05），降低SIRT1表达和CFU-Mix形成能力（P<0.05）。与模型组比较，ASP会抑制衰老HSCs G1期细胞比例、SA-β-Gal染色阳性细胞率、p53及p21蛋白表达增加（P<0.05），同时SIRT1表达增加、CFU-Mix能力增强（P<0.05）。结论ASP可能上调SIRT1表达、下调p53及p21表达，从而可能延缓小鼠HSCs衰老。

Effect of angelica sinensis polysaccharide on expression of SIRT1,p53 and p21 in hematopoietic stem cells

Objective To investigate the effects of angelica sinensis polysaccharide (ASP) based on the expression of HSCs SIRT1, p53 and p21 protein in hematopoietic stem cells (HSCs) of rats with radiation-induced aging, and to discusses possible mechanisms on HSCS aging. Methods Seventy-two SPF grade C57BL / 6J mice were randomly incorporated into the control group, model group and ASP group.The model group was subjected to a mouse HSCs aging model by X-ray 3.0GY/8F system. ASP group was given with ASP during the irradiation. The model and control groups were given with physiological saline. The mouse HSCs were sorted by immunoprugal beads;the cell cycle was detected by flow cytometry; and aging cells were observed by β-galactosidase (Sa-β-Gal) staining. HSCs was observed by mixed colony culture (CFU-Mix)self-update and directional differentiation potential. Western blot was applied for assessing the SIRT1, p53, p21 protein expression. Results Compared to the control group, X-ray irradiation might significantly increase the proportion of the HSCS G1 period, SA-β-Gal staining positive cell ratio, p53 and p21 protein expression (P<0.05), reduce SIRT1 expression and CFU-MIX formation ability in model group (P<0.05). Compared with the model group, ASP significantly suppressed the proportion of aging HSCS G1 cells, increased the expression of SA-β-Gal staining positive cells, p53 and p21 protein (P<0.05); increased and the expression of SIRT1 and CFU-MIX ability (P<0.05). Conclusion The ASP may up-regulate the expression of SIRT1, and down-regulate p53 and p21 expression, which may delay mice HSCs aging.