Abstract

BackgroundAging is characterized by progressive deterioration in metabolic and physiological process. The present research assessed the antagonistic effects and mechanisms of Ginsenoside Rg1 (Rg1) on aging of HSCs/HPCs.Material/MethodsFifty male Sprague-Dawley (SD) rats were treated and divided into the following groups: Control (n=10), Model (n=10, treated with D-galactose, as aging model), Rg1 Control (n=10), Rg1 treatment (n=10), and Rg1 prevention (n=10). An aging rat model was established by subcutaneous injection with D-gal. HSC/HPC cells were stained using SA-β-Gal staining. HSC/HPC cells were examined using flow cytometry assay. CFU-mix assay, with a few modifications, was performed. Cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax) were examined using qRT-PCR. Sirtuin 3 (SIRT3) and superoxide dismutase 2 (SOD2) expression was determined using Western blot assay and qRT-PCR.ResultsRg1 (treatment and prevention group) significantly decreased SA-β-Gal-positive staining in Sca-1+ HSC/HPC cells compared to that of the D-gal model (p<0.05). Rg1 significantly enhanced formation capacity of CFU-Mix compared to the D-gal model (p<0.05) in Sca-1+ HSC/HPC cells. Rg1 significantly reduced G0/G1 phase of Sca-1+ HSC/HPC cells compared to that of the D-gal model (p<0.05). Rg1 significantly decreased cleaved caspase 3 and Bax expression, and increased Bcl-2 expression compared to the D-gal model (p<0.05). Rg1 treatment remarkably upregulated expressions of SIRT3 and SOD2 compared to that of the D-gal model group (p<0.05).ConclusionsRg1 conducted functions of anti-aging in Sca-1+ HSC/HPC cells in the D-gal-induced aging model by inhibiting mitochondrial pathway-mediated apoptosis and activating the SIRT3/SOD2 signaling pathway.

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