Evidence mapPaperPMID 41444626Full record

ArticleStem cell research & therapy2025

Ginsenoside Rh2 inhibits mesenchymal stem cell senescence by regulating mitochondrial and lysosomal function.

Jianjian Zhuang, Yue Li, Yi Ling Huang, Xiang Wang, Neng Ming Lin

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Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

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5 authors.

Jianjian Zhuang *Department 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.
Yue Li *School of Pharmaceutical Sciences, Hangzhou First People's Hospital, Zhejiang Chinese Medical University, Hangzhou, 311402, Zhejiang, China.
Yi Ling HuangSchool of Pharmaceutical Sciences, Hangzhou First People's Hospital, Zhejiang Chinese Medical University, Hangzhou, 311402, Zhejiang, China.
Xiang WangDepartment 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. wangxiang@hospital.westlake.edu.cn.
Neng Ming LinDepartment 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. lnm1013@zju.edu.cn.

Funding

Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province 2020E10021National Natural Science Foundation of China 82204781Zhejiang Provincial Natural Science Foundation of China LQ23H290006Zhejiang Provincial Program for the Cultivation of High-level Innovative Health Talents ZWB-2020-18Zhejiang Provincial Traditional Chinese Medicine Science and Technology Project 2023ZR119
6 · The paper itself

Abstract

backgroundMesenchymal 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.

methodsTransmission 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.

resultsRh2 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.

conclusionThese findings provide a potential strategy for using Rh2 to overcome the senescence of MSCs, thereby enhancing their clinical application.

Indexed as

Cellular SenescenceGinsenosidesLysosomesMesenchymal Stem CellsMitochondriaCells, CulturedHumansProtein KinasesPTEN-Induced Putative KinaseSirtuin 1Ubiquitin-Protein Ligasesginsenoside Rh2Ginsenosidesparkin proteinProtein KinasesPTEN-Induced Putative KinaseSirtuin 1Ubiquitin-Protein LigasesLysosomesMesenchymal stem cellsMitochondriaRh2SenescentSIRT1

Identifiers

PMID41444626
PMCPMC12729120

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.