Life sciencesJul 29, 2018

Ginsenoside Rg1 helps delay aging in bone marrow cells by affecting bone marrow support cells

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 27, 2026

Abstract

Rg1 significantly decreased the percentage of positive cell SA-Gal staining in bone marrow stromal cells (BMSCs) from an aging rat model.

Rg1 treatment reduced the effects of aging on BMSCs by lowering the rate of senescence-associated β-galactosidase (SA-Gal) positive cells.
Increased proliferative ability of BMSCs was observed after Rg1 treatment, indicating enhanced cell growth.
Co-culturing bone marrow nucleated cells (BMNCs) with Rg1-treated BMSCs led to a decreased apoptosis rate and improved mixed colony formation.
In BMNCs, Rg1 treatment resulted in reduced SA-Gal positive cell staining and enhanced colony-forming unit capacity.
Rg1 may restore hematopoietic capacity in BMNCs by counteracting aging effects through multiple pathways.

Simplified

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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Ginsenoside Rg1 helps delay aging in bone marrow cells by affecting bone marrow support cells

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