ArticleEuropean journal of medical research2024
Ginsenoside Rh2 suppresses ferroptosis in ulcerative colitis by targeting specific protein 1 by upregulating microRNA-125a-5p.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- pH-responsive microgels containing multifunctional ginsenoside Rh2-based liposomes remodel intestinal environment to enhance celastrol therapy for ulcerative colitis.Materials today. Bio · 2026Article
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- Ginsenoside-Mediated Ferroptosis Regulation: Bidirectional Effects and Therapeutic Potential in Diseases.International journal of molecular sciences · 2026Review
- MicroRNAs as novel therapeutic targets against inflammatory bowel disease through modulation of ferroptosis.Clinical and experimental medicine · 2026Review
- The Achilles' heel of hepatocellular carcinoma: ginsenoside compound K as a novel GPX4 degrader promotes ferroptosis in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- TLR4/NF-κB-mediated M1 macrophage polarization contributes to the promotive effects of ETS2 on ulcerative colitis.European journal of medical research · 2025Article
- Microbial Fermentation Affects the Structure-Activity Relationship of Bioactive Compounds in Ginseng and Its Applications in Fermentation Products: A Review.Foods (Basel, Switzerland) · 2025Review
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5 authors.
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Abstract
backgroundWorldwide, ulcerative colitis (UC) is becoming increasingly fast growing. Ginsenoside Rh2 has been reported to alleviate UC. However, the latent biological mechanism of Rh2 in the treatment of UC remains uncertain. In this study, the goal was to determine the therapeutic effect of Rh2 on dextran sulfate sodium (DSS)-induced UC.
methodsA DSS-induced UC mouse model was established and divided into 7 groups for Rh2 gavage and/or miR-125a-5p lentivirus injection (n = 10 per group). Colonic specimens were collected for phenotypic and pathological analysis. miR-125a-5p and specific protein 1 (SP1) expression, inflammation-related factors IL-6 and IL-10, and apoptosis were detected in mice. Human normal colon epithelial cell line NCM460 was treated with H
resultsDSS-induced UC mice had significantly decreased body weight, increased disease activity index, decreased colon length, and decreased miR-125a-5p expression (all P < 0.05). In the DSS-induced mouse model, the expression of miR-125a-5p rebounded and ferroptosis was inhibited after Rh2 treatment (all P < 0.05). Inhibition of miR-125a-5p or upregulation of SP1 expression counteracted the protective effects of Rh2 on UC mice and ferroptosis cell models (all P < 0.05).
conclusionsRh2 mitigated DSS-induced colitis in mice and restrained ferroptosis by targeting miR-125a-5p. Downregulating miR-125a-5p or elevating SP1 could counteract the protective impacts of Rh2 on ferroptotic cells. The findings convey that Rh2 has a latent application value in the treatment of UC.
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