ArticleAmerican journal of translational research2021
Deoxyschizandrin treats mice with ulcerative colitis possibly via the TLR4/NF-κB signaling pathway.
Article in American journal of translational research, 2021. 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
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- A comparative study of dextran sodium sulfate-induced and spleen-kidney syndrome-based ulcerative colitis models.Biochemistry and biophysics reports · 2026Article
- Mechanism of Morbidity Based on Ulcerative Colitis: A Review of Traditional Chinese Medicine Treatment of Ulcerative Colitis.International journal of general medicine · 2025Review
- Sishen Pill and its active phytochemicals in treating inflammatory bowel disease and colon cancer: an overview.Frontiers in pharmacology · 2024Review
- Harnessing nature's pharmacy: investigating natural compounds as novel therapeutics for ulcerative colitis.Frontiers in pharmacology · 2024Review
- Luteolin alleviates ulcerative colitis in rats via regulating immune response, oxidative stress, and metabolic profiling.Open medicine (Warsaw, Poland) · 2023Article
- Natural Products Modulate Cell Apoptosis: A Promising Way for the Treatment of Ulcerative Colitis.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the effects and mechanisms of deoxyschizandrin (DSD) on treatment of ulcerative colitis (UC).
methodsThe models of mice with UC were established through dextran sulfate sodium (DSS) administration, and the successful models were treated with DSD. The therapeutic effects of DSD on UC mice were evaluated and its behind mechanisms were analyzed.
resultsAfter DSS induction, the mice showed increased body weight and colon length, worse disease activity index (DAI) and body inflammation, oxidative stress injury and increased apoptosis of colonic epithelial cells, which were remarkably relieved after DSD intervention. Besides, the levels of TLR4, MyD88 and NF-κB in the colon tissues were elevated in UC mouse models, while DSD treatment reduced the levels of these markers.
conclusionDSD can alleviate the symptoms of mice with DSS-induced UC via inhibiting body inflammation, improving oxidative stress and reducing the apoptosis of colonic epithelial cells, which may be attributed to DSD inhibition of the TLR4/NF-κB signaling pathway.
Indexed as
Identifiers
34017577PMC8129281W3161853867What 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.