ArticleStem cell research & therapy2025
Rg1-preconditioned adipose-derived mesenchymal stromal cells alleviate colitis via exosome-mediated Inhibition of macrophage glycolysis through RAS signaling.
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. Cited by 2 papers.
What it found
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- Ginsenoside Rg1 Ameliorates LPS-Induced Sepsis-Associated Lung Injury in Mice via VEGFC/D-VEGFR3 Signaling-Mediated Lymphangiogenesis and Lymphatic Remodeling.The Kaohsiung journal of medical sciences · 2026Article
- Innovative strategies for immune thrombocytopenia treatment: immunomodulatory mechanisms and clinical potential of mesenchymal stem cells.Stem cell research & therapy · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
aimsThe therapeutic potential of adipose-derived mesenchymal stromal cells (ADSCs) in inflammatory bowel disease (IBD) is well established, yet the mechanisms underlying their immunoregulatory effects remain unclear. Ginsenoside Rg1 has been shown to enhance the immunomodulatory properties of ADSCs. Given the key role of macrophages in IBD pathogenesis, this study aimed to explore whether mesenchymal stromal cells (MSCs), particularly following Rg1 pretreatment, alleviate colitis by modulating macrophage immunometabolism. MAIN
methodsIn vitro experiments were performed in RAW264.7 macrophages and NCM460 cell. In vivo experiments were performed in C57BL/6 mice. KEY
findingsRg1 pretreatment upregulated stemness-related genes and downregulated immunogenic markers in ADSCs. In vivo, Rg1-preconditioned ADSCs significantly alleviated DSS-induced colitis and inhibited M1 macrophage polarization by reducing glycolytic activity. Mechanistically, ADSC-derived exosomes delivered miRNAs that suppressed glycolysis and RAS signaling in macrophages, thereby limiting pro-inflammatory polarization and ameliorating colitis. This miRNA is presumed to be miR-574-3p. SIGNIFICANCE: MSCs alleviate experimental colitis by modulating macrophage immunometabolism, and Rg1 pretreatment further enhances this therapeutic potential. This effect may involve exosomal miRNAs that inhibit macrophage glycolysis by suppressing the RAS pathway, one of which is predicted to be miR-574-3p. These results suggest a possible metabolic mechanism underlying MSC-based immunotherapy for ulcerative colitis.
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Registered trials
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.