Ginsenoside Rg1 protects against Sca‑1+ HSC/HPC cell aging by regulating the SIRT1‑FOXO3 and SIRT3‑SOD2 signaling pathways in a γ‑ray irradiation‑induced aging mice model

Aug 9, 2020Experimental and therapeutic medicine

Ginsenoside Rg1 helps protect stem cells from aging caused by gamma-ray radiation by controlling cell survival and antioxidant pathways

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Abstract

Rg1 treatment significantly increased white blood cell, red blood cell, and platelet counts in peripheral blood compared with the γ-ray irradiation group (P<0.05).

Rg1 treatment reduced the senescence of hematopoietic stem cells and progenitor cells in aging mice exposed to γ-ray irradiation.
The percentage of stained cells indicating senescence was significantly lower in the Rg1 group compared to the γ-ray irradiation group (P<0.05).
Rg1 treatment resulted in a significant increase in mixed hematopoietic progenitor cell colony counts compared to the γ-ray irradiation group (P<0.05).
Levels of key proteins and mRNA associated with cellular health, such as SIRT1, SIRT3, FOXO3, and SOD2, were significantly elevated in the Rg1 group (P<0.05).
The proportion of stem cells in the G1 phase of the cell cycle was significantly lower in the Rg1 group compared to the γ-ray irradiation group (P<0.05).

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Aging is characterized by a progressive deterioration in metabolic functions. The present study aimed to investigate the antagonistic effects of ginsenoside Rg1 (Rg1) on the γ-ray irradiation-induced aging of mixed hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs). C57BL/6 mice were divided into a control group, a γ-ray irradiation group that served as an aging mouse model, and an Rg1 group. The Rg1 group was treated with Rg1 at dosage of 20 mg/kg/day for 7 days prior to γ-ray irradiation. The aging mouse model was established by exposing the mice to 6.5-Gy γ-ray total-body irradiation. Stem cell antigen 1 positive (Sca-1) HSC/HPCs isolated from the mice were examined using a senescence-associated β-galactosidase (SA-β-Gal) staining assay. The cell cycle of the HSC/HPCs was examined using flow cytometry. A mixed hematopoietic progenitor cell colony-forming unit (CFU-mix) assay was also conducted. The mRNA and protein expression levels of sirtuin 1 (SIRT1), SIRT3, forkhead box O3 (FOXO3) and superoxide dismutase (SOD2) were evaluated using western blot and reverse transcription-quantitative PCR assays. The results indicated that Rg1 treatment significantly increased white blood cell, red blood cell and platelet counts in peripheral blood compared with those in the γ-ray irradiation group (P<0.05). However, Rg1 significantly attenuated the senescence of Sca-1HSC/HPCs in the γ-ray irradiation aging mice model. The proportion of SA-β-Gal stained HSC/HPCs was significantly decreased and CFU-Mix counts were significantly increased in the Rg1 group compared with the γ-ray irradiation group (P<0.05). Rg1 significantly increased the mRNA and protein levels of SIRT1, SIRT3, FOXO3 and SOD2 in the Sca-1HSC/HPCs compared with those in the γ-ray irradiation group (P<0.05). The percentage of Sca-1HSC/HPCs arrested at the G1 phase in the Rg1 group was significantly decreased compared with that in the γ-ray irradiation group (P<0.05). In conclusion, the present study indicates that Rg1 exerts anti-aging effects via the regulation of SIRT1-FOXO3 and SIRT3-SOD2 signaling pathways, and triggering the progression of Sca-1HSC/HPCs from the G1 phase to the S phase in γ-ray irradiation-induced aging mice. + + + + +

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Ginsenoside Rg1 protects against Sca‑1+ HSC/HPC cell aging by regulating the SIRT1‑FOXO3 and SIRT3‑SOD2 signaling pathways in a γ‑ray irradiation‑induced aging mice model

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