Angelica sinensis Polysaccharides Reduce 5-Fluorouracil-Induced Inhibition on Osteogenic Differentiation of Bone Marrow Stromal Cells
QI Rongjia, XIAO Hanxianzhi, WANG Ziling, DENG Fangfang, WU Qi, WANG Yaping, WANG Lu*
The aim of the study was to investigate the effect of ASP (Angelica sinensis polysaccharides) on ameliorating the imbalance of osteogenic and adipogenic differentiation of human bone marrow stromal cells induced by 5-FU (5-fluorouracil). Human bone marrow stromal cell line HS-5 cells were cultured in vitro and divided into: Control group, ASP group, 5-FU group, 5-FU+ASP group and 5-FU+LiCl group. Cell inhibition rate of HS-5 cells was detected by CCK-8 assay, and the cellular apoptosis was analyzed by flow cytometry. The ability of BMSCs for osteogenesis and adipogenic differentiation was detected by osteogenic and adipogenic differentiation assays. The expressions of Runx2, PPARγ and β-catenin protiens were measured by Western blot. The mRNA expressions of Runx2, OCN, BMP-2, Osterix, PPARγ and β-catenin were detected by RT-PCR. The results indicated that compared with the control group, the proliferative capacity of HS-5 cells was inhibited and the apoptosis rate was increased in the 5-FU group. The osteogenesis potential was decreased whereas adipogenesis potential was enhanced. The mRNA and protein levels of differentiation-related signaling molecule β-catenin were decreased. However, compared with the 5-FU group, the apoptosis rate of HS-5 cells was decreased after ASP pretreatment. The osteogenesis ability of HS-5 was restored while the adipogenesis potential was reduced. The expression of osteogenicrelated factors including Runx2, OCN, BMP-2 and Osterix was increased whereas the expression of the lipid-related factor PPARγ was decreased. The expression of β-catenin was increased in 5-FU+ASP group. The results suggested that Angelica sinensis polysaccharides protected bone marrow stromal cells against 5-FU via maintaining osteogenesis potential, and the underlying mechanism might be related to activating Wnt/β-catenin signaling pathway.