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Rg1 Protects Hematopoietic Stem Cells from LiCl-Induced Oxidative Stress via Wnt Signaling Pathway

BACKGROUND: Ginsenoside Rg1 is a major component of ginseng with antioxidative and antiaging effects, which is a traditional Chinese medicine. In this study, we investigated the potential spillover and mechanism of action of Rg1 on LiCl-driven hematopoietic stem cell aging. RESULTS: Collect the puri...

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Detalles Bibliográficos
Autores principales: Wang, Ziling, Xia, Jieyu, Li, Jing, Chen, Linbo, Chen, Xiongbin, Zhang, Yanyan, Wang, Lu, Wang, Yaping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8977299/
https://www.ncbi.nlm.nih.gov/pubmed/35388306
http://dx.doi.org/10.1155/2022/2875583
Descripción
Sumario:BACKGROUND: Ginsenoside Rg1 is a major component of ginseng with antioxidative and antiaging effects, which is a traditional Chinese medicine. In this study, we investigated the potential spillover and mechanism of action of Rg1 on LiCl-driven hematopoietic stem cell aging. RESULTS: Collect the purified Sca-1(+) hematopoietic cells for differentiation ability detection and biochemical and molecular labeling. The experiment found that Rg1 plays an antiaging role in reversing the SA-β-gal staining associated with LiCl-induced hematopoietic stem cell senescence, the increase in p53 and p21 proteins, and sustained DNA damage. At the same time, Rg1 protects hematopoietic cells from the reduced differentiation ability caused by LiCl. In addition, Rg1 increased the excessive inhibition of intracellular GSK-3β protein, resulting in the maintenance of β-catenin protein levels in hematopoietic cells after LiCl treatment. Then, the target gene level of β-catenin can be maintained. CONCLUSIONS: Rg1 exerts the pharmacological effect of maintaining the activity of GSK-3β in Sca-1(+) hematopoietic cells, enhances the antioxidant potential of cells, improves the redox homeostasis, and thus protects cells from the decline in differentiation ability caused by aging. This study provides a potential therapeutic strategy to reduce stem cell pool failure caused by chronic oxidative damage to hematopoietic stem cells.