ArticleCancer management and research2026
Astragalin Suppresses Colorectal Carcinogenesis by Targeting Proliferation, Oxidative Stress, and Inflammation.
Article in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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: Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide. This study evaluated astragalin's (AST) anti-proliferative and chemopreventive effects on CRC. Methods: AST's effects were assessed in vitro on Caco-2 and HT-29 cells and in vivo on azoxymethane (AOM)-induced aberrant crypt foci (ACF) in rats. Rats received AST (50 or 100 mg/kg, 60 days) or 5-fluorouracil (5-FU) (35 mg/kg, 5 days). Results: AST inhibited Caco-2 and HT-29 cell growth (IC50: 20.15-34.50 µg/mL). In AOM-induced rats, AST reduced ACF formation, improved colon histology, downregulated β-catenin, and upregulated Bax. AST also enhanced superoxide dismutase (SOD) and catalase (CAT) activities, reduced malondialdehyde (MDA) levels, and modulated tumor necrosis factor alpha (TNF-α), interlukin-6 (IL-6), and IL-10 levels. Conclusion: AST demonstrated chemopreventive activity against CRC by exerting antiproliferative, antioxidant, and anti-inflammatory effects, supporting its potential as a therapeutic agent.
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.