ArticleFrontiers in immunology2025
Nrf2/HO-1-dependent inhibition of ferroptosis underlies the antioxidant effects of 5-O-methylvisammioside in colitis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Norcantharidin Ameliorates Experimental Ulcerative Colitis Through Epigenetic and Metabolic Reprogramming Involving IL-6/DNMT1/SOCS3 and AMPK/SIRT1/FOXO3a-Nrf2 Signaling.International journal of molecular sciences · 2026Article
- Immunoprotective Effects of Mori Cortex Radicis Water Extract on Major Aquatic Pathogen (Life (Basel, Switzerland) · 2026Article
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ferroptosis contributes to epithelial injury and chronic inflammation in ulcerative colitis, yet pharmacologic strategies that durably attenuate ferroptosis and restore barrier function remain limited. 5-O-Methylvisammioside (MeV) is a natural compound with putative antioxidant properties, but its anti-colitic mechanisms are unclear. Purpose: To determine whether MeV alleviates colitis by activating the Nrf2/HO-1 axis and constraining ferroptosis. Methods: Acute colitis was induced in male Sprague-Dawley rats using dextran sulfate sodium and animals were randomized to vehicle, DSS alone, two MeV doses, or mesalazine as a benchmark control. Clinical activity, colon length, and histopathology were quantified alongside epithelial barrier readouts (ZO-1, occludin), oxidative stress and ferroptosis markers (lipid reactive oxygen species, malondialdehyde/4-hydroxynonenal, iron accumulation, GPX4, ACSL4), and Nrf2/HO-1 activation, including nuclear translocation of Nrf2. In parallel, erastin-challenged Caco-2 cells were used to test whether MeV directly restrains ferroptosis; Nrf2 knockdown probed pathway dependency. Results: MeV dose-dependently reduced disease activity and histological damage and partially normalized colon length. Barrier proteins were preserved, and lipid peroxidation and iron overload were diminished. MeV increased Nrf2 nuclear translocation and upregulated HO-1, restored GPX4, and lowered ACSL4, consistent with ferroptosis restraint. Conclusion: MeV alleviates experimental colitis, at least in part by activating Nrf2/HO-1 to restrain ferroptosis and preserve epithelial barrier integrity. These findings nominate MeV as a ferroptosis-targeting candidate for colitis.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.