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Ginsenoside Rh2 inhibits mesenchymal stem cell senescence by regulating mitochondrial and lysosomal function
Jianjian Zhuang1,2, Yue Li3, Yi Ling Huang3
1Department of Clinical pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, 310006, Zhejiang, China. zhuangjianjian@hospital.westlake.edu.cn.
Background:
Mesenchymal stem cells (MSCs) undergo senescence after expansion and in vitro culture under oxidative stress, which limits their clinical application. Ginsenoside Rh2 has been confirmed to regulate mitochondrial function, but its role in modulating the senescence of MSCs has not been clearly investigated.
Purpose:
This study aims to explore the effects and underlying mechanisms of Rh2 in inhibiting the senescence of MSCs.
Methods:
Transmission electron microscopey (TEM) and fluorescence staining assays were used to monitor changes in mitochondrial and lysosomal morphology and function in Rh2-treated senescent MSCs. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were performed to evaluate the expression levels of senescence-related cytokine genes and proteins.
Results:
Rh2 can inhibited the senescence of MSCs by activating Sirtuin 1(SIRT1). At the molecular level, SIRT1 regulated the Pink1/Parkin-mediated mitophagy pathway and suppressed the secretion of senescence-associated cytokines (IL-6 and IL-8). Additionally, Rh2 influenced lysosomal stability and sultimately inhibited exosome secretion through direct activation of SIRT1.
Conclusion:
These findings provide a potential strategy for using Rh2 to overcome the senescence of MSCs, thereby enhancing their clinical application.
Insights
Ginsenoside Rh2 inhibits mesenchymal stem cell (MSC) senescence by activating Sirtuin 1 (SIRT1). This process enhances mitochondrial function and reduces inflammatory cytokine secretion, improving MSCs for clinical use.
Area of Science:
- Stem cell biology
- Mitochondrial research
- Aging research
Background:
- Mesenchymal stem cells (MSCs) undergo senescence due to oxidative stress during expansion and in vitro culture, limiting their clinical utility.
- Ginsenoside Rh2 is known to regulate mitochondrial function, but its impact on MSC senescence is not well understood.
Purpose of the Study:
- To investigate the effects of Ginsenoside Rh2 on inhibiting MSC senescence.
- To elucidate the molecular mechanisms by which Rh2 modulates MSC aging.
Main Methods:
- Transmission electron microscopy (TEM) and fluorescence staining to assess mitochondrial and lysosomal changes.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot to analyze senescence-related gene and protein expression.
- Evaluation of cytokine secretion and exosome release.
Main Results:
- Ginsenoside Rh2 inhibited MSC senescence by activating Sirtuin 1 (SIRT1).
- SIRT1 activation by Rh2 promoted Pink1/Parkin-mediated mitophagy and suppressed the secretion of senescence-associated cytokines (IL-6, IL-8).
- Rh2 enhanced lysosomal stability and reduced exosome secretion via direct SIRT1 activation.
Conclusions:
- Ginsenoside Rh2 effectively inhibits MSC senescence through SIRT1 activation.
- This study presents Rh2 as a potential therapeutic strategy to improve MSCs for enhanced clinical applications.
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