ArticleActa cirurgica brasileira2024
Columbianadin ameliorates experimental acute reflux esophagitis in rats via suppression of NF-κB pathway.
Article in Acta cirurgica brasileira, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- ZDHHC5: a pivotal palmitoyltransferase orchestrating signaling networks - unraveling mechanisms and therapeutic horizons.Biomarker research · 2026Review
- Downregulation of MUC6 improves esophageal epithelial barrier dysfunction and inhibits epithelial-mesenchymal transition in reflux esophagitis.BMC gastroenterology · 2026Article
- Stigmasterol, the Active Ingredient in Huanglian Decoction, Inhibits the MAOA-NF-κB-MLCK Pathway to Improve the Inflammation in Rats With Reflux Esophagitis.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Alpinumisoflavone ameliorates experimental acute reflux esophagitis in rats via regulation of inflammatory pathway.Acta cirurgica brasileira · 2025Article
- Integrated transcriptomic and metabolomic analyses reveal the mechanism by which quercetin inhibits reflux esophagitis in rats.PloS one · 2025Article
- Pharmacological and Pharmacokinetic Insights Into Columbianadin: A Promising Natural Anti-Inflammatory Compound.Mediators of inflammation · 2025Review
- Phytochemistry and Biological Profile of the Chinese Endemic Herb GenusMolecules (Basel, Switzerland) · 2024Review
- Hepatoprotective effects of cinnamaldehyde against high-fat diet-induced liver damage.Avicenna journal of phytomedicineArticle
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Authors and funding
3 authors.
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Abstract
purposeReflux esophagitis is a condition characterized by inflammation and irritation of the esophagus, resulting from the backflow of stomach acid and other gastric contents into the esophagus. Columbianadin is a coumarin derivative that exhibits anti-inflammatory and antioxidant effects. In this study, we tried to scrutinize the protective effect of Columbianadin against acute reflux esophagitis in rats.
methodsRAW 264.7 cells were utilized to assess cell viability and measure the production of inflammatory parameters. The rats received anesthesia, and reflux esophagitis was induced via ligation of pylorus and fore stomach and corpus junction. Rats received the oral administration of Columbianadin (25, 50 and 100 mg/kg) and omeprazole (20 mg/kg). The gastric secretion volume, acidity, and pH were measured. Additionally, the levels of oxidative stress parameters, cytokines, and inflammatory markers were determined. At the end of the study, mRNA expression was assessed.
resultsColumbianadin remarkably suppressed the cell viability and production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and prostaglandin (PGE2). Columbianadin treatment remarkably suppressed the secretion of gastric volume, total acidity and enhanced the pH level in the stomach. Columbianadin remarkably altered the level of hydrogen peroxidase, free iron, calcium, and plasma scavenging activity, sulfhydryl group; oxidative stress parameters like malonaldehyde, glutathione, superoxide dismutase, catalase, glutathione peroxidase; inflammatory cytokines viz., TNF-α, IL-6, IL-1β, IL-10, IL-17, and monocyte chemoattractant protein-1; inflammatory parameters including PGE2, iNOS, COX-2, and nuclear kappa B factor (NF-κB). Columbianadin remarkably (P < 0.001) suppressed the mRNA expression TNF-α, IL-6, IL-1β and plasminogen activator inhibitor-1.
conclusionsColumbianadin demonstrated a protective effect against acute reflux esophagitis via NF-κB pathway.
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