ArticleInflammopharmacology2020
Low-dose curcumin reduced TNBS-associated mucin depleted foci in mice by scavenging superoxide anion and lipid peroxides, rebalancing matrix NO synthase and aconitase activities, and recoupling mitochondria.
Article in Inflammopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 23 citations in OpenAlex.
- Host metabolism shapes the intestinal microbiota: a top-down paradigm of environmental selection pressure.Gut microbes · 2026Review
- Curcumin for inflammatory bowel disease therapy: advances in mechanisms, clinical applications, and drug delivery.Archives of pharmacal research · 2025Review
- Pharmacological modulation of mitochondrial function as novel strategies for treating intestinal inflammatory diseases and colorectal cancer.Journal of pharmaceutical analysis · 2025Review
- Advancing Polyphenol-Based Nanomedicine for Inflammatory Bowel Disease: Challenges and Opportunities.Journal of inflammation research · 2024Review
- Pharmacological Mechanisms and Clinical Applications of Curcumin: Update.Aging and disease · 2023Review
- The role of cholesterol and mitochondrial bioenergetics in activation of the inflammasome in IBD.Frontiers in immunology · 2022Review
- First Evidence of a Protective Effect of Plant Bioactive Compounds against HAntioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of mitochondrial dysfunction in the pathogenesis of inflammatory bowel diseases (IBD) is still being investigated. This study evaluated the therapeutic effect of curcumin (Cur), a polyphenolic electrophile in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced chronic colitis and mitochondrial dysfunction, in mice.
methodsColitis was induced by rectal instillation to mice of 30 mg kg
resultsIn vitro, a short-term Cur treatment controlled the dose and time dependent mitochondrial toxicity induced by TNBS, by collapsing the generation of superoxide anion and hydroperoxy lipids, rebalancing nitric oxide synthase and aconitase activities, and recoupling mitochondria. In vivo, a daily low-dose Cur abolished mice mortality which reached 27% in model group. Cur improved in a time dependent manner mucosal redox homeostasis, cell apoptosis, mucin depleted crypts and crypt abscesses by controlling prooxidant activity of myeloperoxidase and NO synthase associated to phagocytes influx, quenching hydroperoxy lipids, and reboosting GSH levels.
conclusionCur, by quenching intra and extra mitochondrial ROS generation, rebalancing aconitase/fumarase and MDA/GSH ratios, and recoupling mitochondria, may support mithormesis priming and remitting in IBD.
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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.