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

    loading  Checking for direct PDF access through Ovid

Abstract

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.

Related Topics

    loading  Loading Related Articles