ArticleInflammopharmacology2025
Anti-inflammatory, anti-colitis, and antioxidant effects of columbianadin against DSS-induced ulcerative colitis in rats via alteration of HO-1/Nrf2 and TLR4-NF-κB signaling pathway.
Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Ulcerative colitis: from molecular pathophysiology to management and the emerging role of natural and pharmacological drug candidates.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Article
- Innovate sodium alginate microneedle patches integrated with soft lidocaine invasomes: advanced strategies for oral ulcerative mucositis treatment via TNF-α/NF-κB pathways.Drug delivery and translational research · 2026Article
- Construction of a nanozyme composite drug delivery system based on columbianadin for inflammatory bowel disease therapy.RSC advances · 2026Article
- Design and biological evaluation of mesalamine-NSAID hybrids targeting the NLRP3 inflammasome: a multi-target strategy for ulcerative colitis therapy.Scientific reports · 2025Article
- Protective Effects of Aucubin in DSS-Induced Colitis: Modulation of Inflammatory Pathways, Intestinal Barrier Integrity, and Gut Microbiota.Foods (Basel, Switzerland) · 2025Article
- Pharmacological and Pharmacokinetic Insights Into Columbianadin: A Promising Natural Anti-Inflammatory Compound.Mediators of inflammation · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUlcerative colitis (UC) is a significant inflammatory bowel disease (IBD) that typically arises from chronic inflammation of the intestinal tract. Report suggest that anti-inflammatory drug plays a crucial role in the protection of UC. The recent study demonstrated that columbianadin has a protective effect against UC induced by dextran sulfate sodium (DSS) in rats through the modulation of HO-1/Nrf2 and TLR4-NF-κB signaling pathways. MATERIAL AND
methodsIn this study, Swiss Wistar rats were utilized, and UC was induced using 2% DSS. The treatment regimen included oral administration of columbianadin (5, 10 and 15 mg/kg) and sulfasalazine to the rats. The body weight, spleen index, disease activity index (DAI), colon length, food and water intake were estimated. Moreover, antioxidant, cytokines, inflammatory and apoptosis parameters were determined. mRNA expression levels were also quantitatively analyzed.
resultsColumbianadin treatment significantly (P < 0.001) boosted the body weight and suppressed the DAI. Columbianadin significantly (P < 0.001) enhanced the colon length and repressed the spleen index along with enhanced food and water intake. Columbianadin significantly (P < 0.001) suppressed the level of lactate dehydrogenase (LDH), myeloperoxidase (MPO) and altered the level of oxidative stress parameters such as catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), malonaldehyde (MDA), nitric oxide (NO), SA; cytokines level such as interleukin (IL)-1, 1β, 6, 10, 17, 18, TNF-α; inflammatory parameters viz., cyclooxygenase-2 (COX-2), prostaglandin (PGE
conclusionColumbianadin exhibited the protective effect against DSS-induced UC via alteration of HO-1/Nrf2 and TLR4-NF-κB signaling pathway.
Indexed as
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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.