The regulation of ginsenoside Rg1 upon aging of bone marrow stromal cell contribute to delaying senescence of bone marrow mononuclear cells (BMNCs)

骨髓 间质细胞 衰老 造血 体内 细胞 外周血单个核细胞 体外 细胞凋亡 化学 细胞生长 细胞生物学 干细胞 间充质干细胞 癌症研究 免疫学 生物 生物化学 生物技术
作者
Yunlin Zeng,Wenxu Hu,Pengwei Jing,Xiong-Bin Chen,Ziling Wang,Lu Wang,Yaping Wang
出处
期刊:Life Sciences [Elsevier]
卷期号:209: 63-68 被引量:9
标识
DOI:10.1016/j.lfs.2018.07.025
摘要

To investigate the effect and mechanism of ginsenoside Rg1 antagonizing bone marrow stromal cells (BMSCs) aging, which contribute to the delaying senescence of hematopoietic cells in vitro and in vivo. Rg1 could reduce the effects of senility agent on BMSCs by decreasing the rate of SA-Gal positive cells, and increasing the proliferative ability of CCK8 cells. After BMNCs co-cultured with BMSCs which were treated by Rg1 in vitro, compared with BMNCs co-cultured with BMSCs from aging group, percentage of positive cell SA-Gal staining was decreased, the formation ability of CFU-Mix was enhanced, the proliferative ability was increased, and the apoptosis rate was decreased. In aging rat model, after treated with Rg1, the percentage of positive cell SA-Gal staining in BMSCs was significantly decreased, the proliferative ability was increased. After treated with Rg1, the percentage of positive cell SA-Gal staining in BMNCs was significantly decreased, the formation ability of CFU-Mix mixed colony was enhanced, ROS was decreased, and SOD activity was increased. Aging BMSCs could induce the senescence of BMNCs. Rg1 could antagonize the effect of d-gal on the aging of BMSCs both in vivo and in vitro, and restore the hematopoietic capacity of BMNCs through the different pathways.
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