Evidence map›Paper›PMID 42583981›Full record

ArticleIndian journal of pharmacology2026

Rice bran extract ameliorates experimental colitis by modulating gut dysbiosis and toll-like receptor 4/nuclear factor kappa β signaling.

Hagar M Shendy, Omneya Galal, Walaa Wadie, Nourtan F Abdeltawab, Amr Helal, Mohamed T Khayyal, Sarah S Mohamed

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Article in Indian journal of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Hagar M ShendyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Egypt.
Omneya GalalDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ahram Canadian University, Egypt.
Walaa WadieDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Egypt.
Nourtan F AbdeltawabDepartment of Microbiology and Immunology, Faculty of Pharmacy, Cairo University, Egypt.
Amr HelalHealth Tech, Egypt.
Mohamed T KhayyalDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Egypt.
Sarah S MohamedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGut dysbiosis is widely recognized to serve as crucial role in the etiology of inflammatory bowel disease (IBD). This research evaluates the ability of a stabilized rice bran extract (RBE) to modulate positively microbial dysbiosis in an experimentally induced IBD model. MATERIALS AND

methodsRats were given 5% dextran sulfate sodium (DSS) in drinking water during a week to cause colitis. RBE was administered to the rats with a daily dosage of 100 mg/kg, 1 week before feeding them with DSS and continued during DSS treatment. Fecal samples were then collected to assess alterations in the chosen microbial phyla, while colon samples were processed for histological and biochemical assessment.

resultsThe colonic expression of toll-like receptor 4 (TLR4), nuclear factor kappa β (NF-κB), tumor necrosis factor alpha, and interlukin-17 (IL-17) was significantly elevated when DSS induced colitis, resulting in significant histopathological damage and a decrease in the amount of IL-10. Furthermore, DSS caused the colonic tight junction (TJ) protiens mRNA expression to drop dramatically. All undesirable changes induced by DSS tended to be reversed by RBE. Moreover, RBE beneficially modulated the gut microbiota by restoring various bacteria to their normal levels.

conclusionsThe current research demonstrated the potential protective effect of RBE against colonic inflammation through modulating microbiota dysbiosis, TJ protein dysfunction, and TLR4/NF-κB signaling.

Indexed as

ColitisDysbiosisNF-kappa BOryzaPlant ExtractsToll-Like Receptor 4AnimalsColonDextran SulfateDisease Models, AnimalGastrointestinal MicrobiomeMaleRatsSignal TransductionDextran SulfateNF-kappa BPlant ExtractsTlr4 protein, ratToll-Like Receptor 4ColitisDSSdysbiosismicrobiotarice brantight junction

Identifiers

PMID42583981
PMCPMC13412436

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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.