Ginsenoside Rg1 delays the senescence of adipose-derived stem cells: network pharmacology and experimental validation.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

BACKGROUND: Mesenchymal stem cell (MSC) senescence limits their therapeutic potential. Adipose-derived stem cells (ADSCs), though easily accessible, are prone to senescence under oxidative or inflammatory stress. Ginsenoside Rg1, with antioxidant and anti-inflammatory properties, may counteract this process. This study investigates whether Rg1 can alleviate ADSC senescence and its underlying mechanisms. METHODS: To explore the molecular mechanisms by which Ginsenoside Rg1 mitigates ADSC senescence, network pharmacology and molecular docking were applied to identify potential signaling pathways and targets. Cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay to select the optimal modeling concentration. Flow cytometry was used to analyze cell cycle distribution and immune-related marker expression in ADSCs. Reverse transcription quantitative PCR (RT-qPCR) quantified stemness- and senescence-related gene expression. Immunofluorescence (IF) staining assessed senescence-associated protein levels. Western blotting (WB) was performed to examine key proteins in the PI3K/AKT signaling pathway. RESULTS: Network pharmacology identified 22 aging-associated genes targeted by Rg1, with AKT1 emerging as a central hub protein exhibiting high binding affinity. In hydrogen peroxide (H₂O₂)-induced senescence model, Rg1 treatment significantly enhanced cell viability and stemn

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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