ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Repurposing alogliptin for ulcerative colitis: involvement of MicroRNAs, anti-inflammatory, and barrier-restoring mechanisms.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Chemical Characterization, Network Pharmacology, Molecular Docking, and Comparative Anti-Colitic Activity of Polar and Nonpolar Fractions From Raphanus Sativus L. Seeds.Chemistry & biodiversity · 2026Article
- Protective Effects of Sitagliptin on Dextran Sulfate Sodium-Induced Colitis via Modulation of Inflammatory and Oxidative Stress.Medicina (Kaunas, Lithuania) · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis (UC) is a chronic immune-mediated inflammatory bowel disease characterized by persistent mucosal inflammation, oxidative stress, and epithelial barrier disruption. Despite current therapies, achieving sustained mucosal healing remains difficult, highlighting the need for agents that modulate overlapping immune and oxidative pathways. This study evaluated the prophylactic effects of alogliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, in acetic acid-induced UC in rats, focusing on microRNA (miRNA) regulation, cytokine balance, and barrier restoration. Forty-eight male Wistar rats were assigned to six groups: control, alogliptin-only, UC, UC + sulfasalazine, UC + alogliptin (10 mg/kg), and UC + alogliptin (20 mg/kg). UC induction caused severe colonic damage with elevated pro-inflammatory cytokines (TNF-α, IL-6, IL-17), and adhesion molecules (VCAM-1, ICAM-1), together with a significant rise in malondialdehyde (MDA), a key pro-oxidative lipid peroxidation marker, reduced IL-10, diminished antioxidant enzymes (SOD, CAT), and decreased tight-junction proteins (ZO-1, Occludin). Alogliptin markedly attenuated histopathological injury and ulcer index, restored redox homeostasis and rebalanced immune signaling by suppressing TNF-α/IL-17 and enhancing IL-10 expression. It also downregulated ADAM-17 and upregulated HO-1, conferring possible immunoregulatory cyto-protection. Moreover, alogliptin -at higher doses- modulated miR-145, miR-200a, and miR-34a, linking microRNA control to its anti-inflammatory and barrier-preserving effects. These findings reveal alogliptin's microRNA-driven anti-inflammatory, antioxidant and mucosal-protective mechanisms, supporting its repurposing as a DPP-4 inhibitor with therapeutic promise in ulcerative colitis.
Indexed as
Identifiers
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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.