Objective  To investigate the effect of Angelica Sinensis polysaccharide (ASP) on proliferation, differentiation and transplantation of human leukemia stem cells(LSCs).   Methods  1. Effect of angelica sinensis polysaccharides on proliferation of CD34⁺CD38^-human LSCs in vitro. By using immunomagnetic bead sorting, CD34⁺CD38^-cells isolated from the bone marrow of normal persons and myeloid leukemia patients were divided into normal CD34⁺CD38^-group, CD34⁺CD38^-LSCs group, CD34⁺CD38^-ASP group and CD34⁺CD38^-LSCs ASP group. The latter two groups were added ASP (terminal concentration 40 mg/L) on the basis of conventional culture. The purity of CD34⁺CD38^-cells was detected by flow cytometry. The viability of cells was detected by trypan blue staining. The proliferation of CD34+CD38-cells were detected by cell counting kit 8(CCK-8) and colony forming unit-mixture (CFU-Mix). The expression of aging-related gene was detected by RT-PCR. 2. Effect of Angelica Sinensis polysaccharide on mouse model of LSCs transplantation. After to establish CD34⁺CD38^-LSCs transplantation mice model, the mice were randomly divided into ASP transplantation model group (intraperitoneal injection with ASP,  200 mg/kg, Qd×14 days) and transplantation model group (intraperitoneal injection with the same volume of saline at the same time). On the 2nd day after drug injection was finished, leukocytes count and classification and cells morphology were observed. By using immunofluorescence cytochemistry, CD34⁺CD38^-LSCs in bone marrow of recipient mice was detected. The percentage of senescence assosiated β-galactosidase(SA-β-Gal) positive staining cells in bone marrow mononuclear cells (BMMCs) was detected. Cell cycle distribution of BMMCs was detected by flow cytometry. The colony formation ability of BMMCs was detected by CFU-Mix.  ResultsThe purity of CD34⁺CD38^- cells was (91.14±1.02)% and the viability of cells was (95.42±3.52)%. The proliferation and CFU-Mix formation ability of CD34⁺CD38^-LSCs group were significantly higher than that of normal CD34⁺CD38^-group. The proliferation and CFU-Mix formation ability of CD34⁺CD38^- LSCs ASP group were obviously lower than that of CD34⁺CD38^-LSCs group. The expressions of p16^INK4a, p19Arf, p53, p21^Cip1/Waf1 genes in CD34⁺CD38^-LSCs ASP group increased. Human LSCs existed in the bone marrow of recipient mice transplanted LSCs. The count of leukocytes in the transplantation model group increased, the proportion of neutrophils increased and lymphocytes decreased. After injection of ASP, the count of leukocytes and the proportion of neutrophils were markedly reduced, meanwhile, the proportion of lymphocytes increased. The number of BMMCs in G₀/G₁ phase increased and in S phase decreased. The percentage of SA-β-Gal positive staining cells increased significantly; the number of CFU-Mix decreased.  Conclusion  ASP inhibits the proliferation of CD34⁺CD38^-LSCs in vivo or in vitro. It is suggested that the mechanism is closely related to the expression of genes related to the regulation of cellular senescence.