[Mechanism of ginsenoside Rg1 in the delayed senescence of hematopoietic stem cell].

Jan 13, 2011Zhonghua yi xue za zhi

How Ginsenoside Rg1 May Slow Aging in Blood-Forming Stem Cells

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Abstract

The percentage of senescent hematopoietic stem cells in the Rg1 treatment group was 21.5% ± 2.8%, significantly lower than the aged group at 69.5% ± 5.0%.

Ginsenoside Rg1 treatment reduced the number of senescent cells and altered cell cycle distribution in hematopoietic stem cells.
The number of mixed hematopoietic progenitor colonies increased from (3.0 ± 1.6)/10(4) in the aged group to (9.2 ± 1.8)/10(4) in the Rg1 delayed aged group.
Rg1 treatment resulted in lower expression of senescence markers such as p16(INK4a) and p21(Cip1/Waf1) compared to aged controls.
Conversely, proteins associated with cell cycle progression, including CDK4, CDK2, and cyclinE, were up-regulated in the Rg1 treatment groups.
The signaling pathways involving p16(INK4a)-Rb and p19(Arf)-p53-p21(Cip/Waf1) may be important in the effects observed with Rg1.

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OBJECTIVE: To investigate the underlying mechanism of ginsenoside Rg1 in the regulation of hematopoietic stem cell (HSC) senescence so as to provide the theoretic and experimental foundations for searching the methods of how to delay its senescence.

METHODS: Sca-1(+)HSC was isolated by magnetic cell sorting (MACS) and divided into control, aged, Rg1, Rg1 treatment aged and Rg1 delayed aged groups. The cellular changes were observed by senescence-associated β-galactosidase (SA-β-Gal) staining. And cell cycle assay and culture of mixed hematopoietic progenitor cell were used to investigate the effect of ginsenoside Rg1 to delay Sca-1(+)HSC senescence. The expressions of p16(INK4a), p19(Arf), p53 and p21(Cip1/Waf1) mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of p16(INK4a), p21(Cip1/Waf1), cyclinD1, cyclinE, CDK2 and CDK4 protein were examined by Western blot.

RESULTS: In the Rg1 treatment and delayed aged groups, the percentage of positive SA-β-Gal-expressing cells was lower than that of the aged group [30.1% ± 2.4%, 21.5% ± 2.8% vs 69.5% ± 5.0%]; the number of cells in G(1) phase was lower than that of the aged group [81.4% ± 1.2%, 78.2% ± 1.4% vs 87.5% ± 4.0%]; but the number of colony for the mixed hematopoietic progenitor was higher than that of the aged group [(8.0 ± 2.2)/10(4) Sca-1(+)HSC, (9.2 ± 1.8)/10(4) Sca-1(+)HSC vs (3.0 ± 1.6)/10(4) Sca-1(+)HSC]. As compared with the aged group, the expressions of p16(INK4a), p19(Arf), p53, p21(Cip1/Waf1)mRNA and p16(INK4a), p21(Cip1/Waf1), cyclinD1 protein were down-regulated (all P < 0.01) while the expressions of CDK4, CDK2 and cyclinE protein up-regulated in Rg1 treatment aged and Rg1 delayed aged groups (all P < 0.01). The changes of the Rg1 delayed aged group were significantly marked than those of the Rg1 treatment aged group.

CONCLUSIONS: Rg1 can effectively delay the t-BHP-induced senescence of HSCs. Both p16(INK4a)-Rb and p19(Arf)-p53-p21(Cip/Waf1) may play an important role in the signaling pathway.

[Mechanism of ginsenoside Rg1 in the delayed senescence of hematopoietic stem cell].

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