ArticleFrontiers in pharmacology2025
Article in Frontiers in pharmacology, 2025. 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.
- [1,3-dicaffeoylquinic acid mitigates dextran sulfate sodium-induced colitis in mice by alleviating oxidative stressNan fang yi ke da xue xue bao = Journal of Southern Medical University · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Materials and Methods: Key components of CAE were identified through ultra-performance liquidchromatography, and their potential targets and pathways were predicted through network pharmacology and molecular docking. The therapeutic effects of CAE were evaluated in a dextran sulfate sodium-induced UC mouse model by assessing clinical parameters, colon length, histopathology, and the expression of inflammatory, tight junction, and apoptosis-related markers. Results: The components of CAE, including chlorogenic acid, kaempferol 3-O-rhamnoside, 1,3-dicaffeoylquinic acid, 3,5-dicaffeoylquinic acid, and 4,5-dicaffeoylquinic acid, were identified. These components interacted with critical targets, including tumor necrosis factor, interleukin-6, interleukin-1β, caspase-3, and Bcl-2, modulating inflammatory and apoptotic pathways. Conclusion: CAE alleviates dextran sulfate sodium-induced colitis by exerting anti-inflammatory and anti-apoptotic effects and maintaining intestinal barrier integrity. These findings support the potential of CAE as a natural multitarget therapeutic agent for UC.
Indexed as
Identifiers
What 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.