ArticleInflammopharmacology2025
Gastroprotective effect of nifuroxazide against indomethacin-induced gastric ulcers in rats via modulation of Nrf2/HO-1, HMGB1/TLR4/NF-κB p65, and apoptotic caspase-3 signaling pathways.
Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Synthesis, Cytotoxicity and Antimicrobial Action of 11 Analogs of Nifuroxazide.International journal of molecular sciences · 2026Article
- The synergistic protective effects of bioactive catechins in longjing tea: alleviate indomethacin-induced gastric toxicity through modulation of inflammatory and apoptotic pathways.Frontiers in pharmacology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
backgroundGastric ulcer (GU) is a common gastrointestinal disease linked to the consumption of non-steroidal anti-inflammatory drugs (NSAIDs), with traditional therapies often causing several adverse effects and drug interactions.
aimThe primary aim of this study was to assess the protective effects of nifuroxazide at three different doses against indomethacin-induced GU.
methodsRats were pretreated orally once daily for 14 days with either nifuroxazide (10, 20, or 40 mg/kg) or famotidine (25 mg/kg), the standard reference drug. After 24 h of fasting, a single oral dose of 50 mg/kg indomethacin was used to induce GU. Six hours later, rats were anesthetized using ketamine.
resultsNifuroxazide dose-dependently mitigated the rise in ulcer index, retained gastric mucin content, and alleviated histopathological changes. These gastroprotective effects were due to the attenuation of oxidative stress, evidenced by reduced malondialdehyde (MDA) levels and increased levels of reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Furthermore, nifuroxazide lessened gastric mucosal inflammation by lowering gastric high mobility group box 1 protein (HMGB1), nuclear factor kappa B p65 (NF-κB p65), tumor necrosis factor-alpha (TNF-α), and signal transducer and activator of transcription 3 (STAT3) levels, toll-like receptor 4 (TLR4) and interleukin-1 beta (IL-1β) expressions, as well as serum levels of C-reactive protein (CRP). In addition, nifuroxazide mitigated apoptosis by inhibiting immunohistochemical expression of caspase-3.
conclusionsNifuroxazide has the potential to be repurposed as a novel gastroprotective therapy that restores gastric mucosal barrier integrity via the mitigation of gastric oxidative stress, inflammation, and apoptosis.
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