ArticleApplied biochemistry and biotechnology2026
Cyanidin-3,5-O-Glucoside Alleviates DSS-Induced Colon Barrier Dysfunction and Fibrosis Through Autophagy-Associated Pathway-Mediated Inflammation Repression in a C57BL/6J Mouse Model.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Rhamnocitrin Ameliorates the Intestinal Fibrosis in DSS-Induced Colitis Mice by Modulating Host-Metabolites and Remodeling the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
The aim of the present study was to investigate the effects of cyanidin-3,5-O-glucoside (C35G) on intestinal inflammation, mucosal barrier integrity, and fibrogenesis in a dextran sodium sulfate (DSS, 2.5%)-induced mouse model of ulcerative colitis (UC), as well as to elucidate the mechanisms underlying its effects. After a 28-day C35G intervention, UC mice showed significant improvements in clinical symptoms, including weight loss and an increased disease activity index (DAI). Additionally, there was an elevation in serum levels of inflammatory factors such as IL-1β, IL-6, IL-17 A, IL-18, and TNF-α. C35G increased the colonic mRNA levels of Zo1, Claudin1, and Occludin, and reduced intestinal epithelial permeability, ultimately promoting the restoration of mucosal barrier integrity in UC mice. In addition, C35G influenced the colonic Nrf2/Keap1 pathway by upregulating the mRNA levels of Cat, Sod1, Sod2, and Mgst1. This modulation was accompanied by an increase in the serum levels of SOD and catalase, as well as a reduction in the levels of the oxidative stress marker MDA. The C35G-induced inhibition of NLRP3 inflammasome activation reduced the expression of intestinal fibrotic factors (α-SMA and Collagen I), ultimately attenuating intestinal fibrosis. Moreover, C35G stimulated autophagy in the intestinal epithelial tissues of UC mice by increasing the protein expression of LC3-II, Beclin 1, p-AMPK, and ULK1 while decreasing the levels of p62, p-Akt, and p-mTOR. These results suggested that C35G reduces oxidative stress and inflammation by acting as an antioxidant and modulating the Nrf2/Keap1 pathway. Additionally, C35G regulates autophagy through the AMPK/Akt/mTOR/ULK1 pathway, thereby improving intestinal inflammation, restoring the compromised intestinal barrier, and preventing intestinal fibrosis in mice with UC.
Indexed as
Identifiers
41484750What Socratic 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 Socratic graph.