Ginsenoside Rg1 enhances the resistance of hematopoietic stem/progenitor cells to radiation-induced aging in mice

Dec 17, 2013Acta pharmacologica Sinica

Ginsenoside Rg1 helps blood stem cells resist radiation-related aging in mice

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Abstract

Irradiation caused a dramatic reduction in the number of Sca-1(+) hematopoietic stem/progenitor cells in mice on day 1.

The number of Sca-1(+) HSC/HPCs was significantly lower on day 1 post-irradiation compared to the sham-irradiated group, with minimal recovery by day 7.
Irradiation resulted in decreased superoxide dismutase (SOD) activity, increased malondialdehyde (MDA) levels, and induced DNA damage in Sca-1(+) HSC/HPCs.
Senescence-related markers showed increased expression of P16(INK4a) and P21(Cip1/Waf1), along with elevated senescence-associated β-galactosidase (SA-β-gal) staining post-irradiation.
Ginsenoside Rg1 administration led to a small but significant recovery in the number of Sca-1(+) HSC/HPCs on days 3 and 7.
Rg1 treatment significantly mitigated the irradiation-induced oxidative stress, DNA damage, and cellular senescence changes in Sca-1(+) HSC/HPCs.

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AIM: To investigate the effects of ginsenoside Rg1 on the radiation-induced aging of hematopoietic stem/progenitor cells (HSC/HPCs) in mice and the underlying mechanisms.

METHODS: Male C57BL/6 mice were treated with ginsenoside Rg1 (20 mg·kg(-1)·d(-1), ip) or normal saline (NS) for 7 d, followed by exposure to 6.5 Gy X-ray total body irradiation. A sham-irradiated group was treated with NS but without irradiation. Sca-1(+) HSC/HPCs were isolated and purified from their bone marrow using MACS. DNA damage was detected on d 1. The changes of anti-oxidative activities, senescence-related markers senescence-associated β-galactosidase (SA-β-gal) and mixed colony-forming unit (CFU-mix), P16(INK4a) and P21(Cip1/Waf1) expression on d 7, and cell cycle were examined on d 1, d 3, and d 7.

RESULTS: The irradiation caused dramatic reduction in the number of Sca-1(+) HSC/HPCs on d 1 and the number barely recovered until d 7 compared to the sham-irradiated group. The irradiation significantly decreased SOD activity, increased MDA contents and caused DNA damage in Sca-1(+) HSC/HPCs. Moreover, the irradiation significantly increased SA-β-gal staining, reduced CFU-mix forming, increased the expression of P16(INK4a) and P21(Cip1/Waf1) in the core positions of the cellular senescence signaling pathways and caused G1 phase arrest of Sca-1(+) HSC/HPCs. Administration of ginsenoside Rg1 caused small, but significant recovery in the number of Sca-1(+) HSC/HPCs on d 3 and d 7. Furthermore, ginsenoside Rg1 significantly attenuated all the irradiation-induced changes in Sca-1(+) HSC/HPCs, including oxidative stress reaction, DNA damage, senescence-related markers and cellular senescence signaling pathways and cell cycle, etc.

CONCLUSION: Administration of ginsenoside Rg1 enhances the resistance of HSC/HPCs to ionizing radiation-induced senescence in mice by inhibiting the oxidative stress reaction, reducing DNA damage, and regulating the cell cycle.

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Ginsenoside Rg1 enhances the resistance of hematopoietic stem/progenitor cells to radiation-induced aging in mice

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