ArticleActa pharmacologica Sinica2011
A protective effect of melatonin on intestinal permeability is induced by diclofenac via regulation of mitochondrial function in mice.
Article in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
- Nocturnal Melatonin Deficiency in Colorectal Cancer: Independent Predictive Value Beyond Sleep Quality.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Exogenous melatonin alleviates premature ovarian failure by regulating granulosa cell autophagy.NPJ Regenerative medicine · 2025Article
- Exploring the Interplay Between Gut Microbiota and the Melatonergic Pathway in Hormone Receptor-Positive Breast Cancer.International journal of molecular sciences · 2025Article
- Enteric-Coated Aspirin Induces Small Intestinal Injury via the Nrf2/Gpx4 Pathway: A Promising Model for Chronic Enteropathy.Drug design, development and therapy · 2025Article
- Effect of melatonin on male offspring testis and sperm parameters in BALB/c mice after exposing their mother to METHamphetamine during pregnancy and lactation.Iranian journal of basic medical sciences · 2023Article
- The relationship between night shift work and breast cancer incidence: A systematic review and meta-analysis of observational studies.Open medicine (Warsaw, Poland) · 2022Article
- Activating Transcription Factor 3 Protects against Restraint Stress-Induced Gastrointestinal Injury in Mice.Cells · 2021Article
- High-salt diet mediates interplay between NK cells and gut microbiota to induce potent tumor immunity.Science advances · 2021Article
- Review
- Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model.Journal of visualized experiments : JoVE · 2021Article
- Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac.Cells · 2020Article
- Melatonin restores the osteoporosis-impaired osteogenic potential of bone marrow mesenchymal stem cells by preserving SIRT1-mediated intracellular antioxidant properties.Free radical biology & medicine · 2020Article
- Ghrelin Attenuates Intestinal Barrier Dysfunction Following Intracerebral Hemorrhage in Mice.International journal of molecular sciences · 2016Article
- Alterations in enterocyte mitochondrial respiratory function and enzyme activities in gastrointestinal dysfunction following brain injury.World journal of gastroenterology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThis study investigated the effect of intragastrically administered melatonin on intestinal mucosal permeability induced by diclofenac in mice.
methodsIntestinal mucosal permeability was induced in mice by intragastric administration of diclofenac (2.5 mg/kg). Melatonin was given intragastrically (10 mg/kg) once per day for 3 d after diclofenac administration. The small intestine was examined macroscopically and microscopically for pathologic injury to the intestinal mucosa. Intestinal mucosal permeability was evaluated by Evans blue and FITC-dextran methods. Mitochondrial functional parameters, including mitochondrial membrane potential, mitochondrial ATPase and succinate dehydrogenase (SDH) activity, were assessed. The malondialdehyde (MDA) and myeloperoxidase (MPO) levels were determined from small intestinal mucosal homogenates.
resultsAs compared with control mice, the permeability, pathologic score, MDA and MPO levels and ulceration of the intestinal mucosa were increased significantly by diclofenac treatment, and a broadened junctional complex and enlarged intercellular space were observed by transmission electron microscopy (TEM). Melatonin treatment significantly reduced the intestinal mucosal permeability, pathologic score, MDA, and MPO levels and ulceration of the intestinal mucosa. By TEM, the small intestine villus morphology and intercellular spaces were nearly normal in melatonin-treated mice. At the level of the mitochondria, melatonin treatment significantly restored the activities of ATPase and SDH.
conclusionThe intestinal damage and increased intestinal permeability induced by diclofenac in mice was limited by melatonin; moreover, melatonin preserved several aspects of mitochondrial function.
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