ArticleInternational journal of molecular sciences2022
Preventive Effect of Vitamin C on Dextran Sulfate Sodium (DSS)-Induced Colitis via the Regulation of IL-22 and IL-6 Production in Gulo(-/-) Mice.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Gut Microbiota Remodeling Mediates the Therapeutic Effects of a Plant-Based Medicine on DSS-Induced Ulcerative Colitis in Mice via the Butyrate-SVCT1-Vitamin C Axis.International journal of molecular sciences · 2026Article
- Cisplatin Induces Inflammation by Activating IL-6 via Suppressing rno-let-7g-5p and rno-let-7f-5p Expression in Intestinal Epithelial Cells.International journal of medical sciences · 2026Article
- Impact of Anaerobic Fermentation Liquid on Bok Choy and Mechanism of Combined Vitamin C from Bok Choy and Allicin in Treatment of DSS Colitis.Foods (Basel, Switzerland) · 2025Article
- Method of oral delivery affects vitamin C-mediated alleviation of colitis in a mouse model.Gut microbes reports · 2025Article
- Anti-Inflammatory Effects of Aptamin C in Pulmonary Fibrosis Induced by Bleomycin.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Aptamin C enhances anti-cancer activity NK cells through the activation of STAT3: a comparative study with vitamin C.Anatomy & cell biology · 2024Article
- Review
- New Insights of Biological Functions of Natural Polyphenols in Inflammatory Intestinal Diseases.International journal of molecular sciences · 2023Review
- Antioxidants as Protection against Reactive Oxidative Stress in Inflammatory Bowel Disease.Metabolites · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS), which are exceptionally high in IBD lesions, are known to cause abnormal immune responses to inflammatory reactions in inflammatory bowel diseases (IBD) through damage to the intestinal mucosal linings. Moreover, they are theorized to be an agent of IBD development. Vitamin C is widely known to be an effective antioxidant for its ability to regulate inflammatory responses through its ROS scavenging effect. Therefore, we examined vitamin C's influence on the development and progression of IBD in Gulo(-/-) mice, which cannot synthesize vitamin C like humans due to a defect in the expression of L-gulono-γ-lactone oxidase, an essential enzyme for vitamin C production. First, we found extensive oxidative stress and an inflammation increase in the colon of vitamin C-insufficient Gulo(-/-) mice. We also found decreased IL-22 production and NKp46(+) cell recruitment and the impaired activation of the p38MAPK pathway. Additionally, comparing vitamin C-insufficient Gulo(-/-) mice to vitamin C-sufficient Gulo(-/-) mice and wild-type mice, the insufficient group faced a decrease in mucin-1 expression, accompanied by an increase in IL-6 production, followed by the activation of the STAT3 and Akt pathways. The results suggest that vitamin C insufficiency induces severe colitis, meaning vitamin C could also take on a preventative role by regulating the production of cytokines and the induction of inflammation.
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