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Published on: July 10, 2019
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.
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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