The positive effects of Ginsenoside Rg1 upon the hematopoietic microenvironment in a D-Galactose-induced aged rat model

Abstract

Background

Ginsenoside Rg1 (Rg1) is one of the most active ingredients in Panax ginseng and has been proven to have anti-oxidative and anti-aging properties. However, there have been few reports concerning the anti-aging effects of Rg1 on the hematopoietic microenvironment and bone marrow stromal cells (BMSCs).

Methods

Thirty Sprague-Dawley rats were randomly divided into four groups (control, D-galactose (D-gal)-administration, Rg1-treatment, and D-gal-administration + Rg1-treatment groups). After D-gal and Rg1 treatment, BMSCs were extracted from femoral bone marrow for culture. After three passages, BMSCs were tested by senescence-associated β-galactosidase (SA-β-gal) staining, flow cytometric cell cycle phase distribution assay, CCK-8 cell proliferation assay, oxidative stress (reactive oxygen species [ROS], superoxide dismutase [SOD], and malondialdehyde [MDA]) assays, inflammatory marker (interleukin (IL)-2, IL-6, and tumor necrosis factor (TNF)-α) enzyme-linked immunosorbent assay (ELISA), stem cell factor (SCF) ELISA, and senescence-associated protein (p16, p21, and p53) Western blotting.

Results

Compared to the D-gal-administration group, the D-gal-administration + Rg1-treatment group showed significantly decreased levels of SA-β-gal + cell %, ROS, MDA, inflammatory marker expression, and senescence-associated protein expression as well as significantly increased levels of S-phase %, cell proliferation, SOD activity, and SCF expression. Compared to controls, the Rg-1-treatment group displayed significantly reduced levels of SA-β-gal + cell %, G1 phase %, ROS, MDA, inflammatory marker expression, senescence-associated protein expression, and SCF expression as well as significantly increased levels of S-phase %, cell proliferation, and SOD activity.

Conclusions

Rg1 improves the anti-aging ability of hematopoietic microenvironment through enhancing the anti-oxidant and anti-inflammatory capacities of BMSCs.