ArticleACS omega2025
Naringenin Alleviates the Autophagy-Associated AMPK-Akt/mTOR Pathway to Regulate Inflammation and Barrier Function, Decreasing DSS-Induced Intestinal Fibrosis.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Supernatants of Water Extraction-Ethanol Precipitation from Roots ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Rhamnocitrin Ameliorates the Intestinal Fibrosis in DSS-Induced Colitis Mice by Modulating Host-Metabolites and Remodeling the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Article
- From Chronic Inflammation to Cancer: The Role of Trained Immunity in IBD-Associated Colorectal Carcinogenesis.Medical sciences (Basel, Switzerland) · 2026Review
- Pharmacology-Driven Dissection of Core Component Sets of Xuefu Zhuyu Decoction in Blood Stasis-Related Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mechanistic Modulation of Autophagy by Bioactive Natural Products: Implications for Human Aging and Longevity.Nutrients · 2026Review
- 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.Applied biochemistry and biotechnology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of strictures due to intestinal fibrosis remains a significant clinical challenge in patients with ulcerative colitis (UC). The purpose of this experiment was to investigate the protective effects of naringenin (NAR, 40 mg/kg), a natural flavonoid predominantly present in grapes and oranges, against dextran sodium sulfate (DSS, 2.5%)-induced intestinal fibrosis in UC mice. Oral administration of NAR effectively mitigated clinical symptoms and histological damage in UC mice by reducing the colonic F4/80 and MPO levels. Additionally, NAR lowered the serum concentrations of proinflammatory cytokines and inhibited NLRP3 inflammasome activation in the colon. NAR regulates the Nrf2/Keap1 pathway to combat oxidative damage caused by DSS and enhance autophagy through the AMPK-Akt/mTOR pathway, ultimately decreasing intestinal fibrosis in UC mice by inhibiting α-SMA and Collagen-I. Taken together, our findings demonstrate that NAR can prevent the occurrence and progression of intestinal fibrosis. This effect is achieved by adjusting the AMPK-Akt/mTOR pathway and the promotion of autophagy at the molecular level.
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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.