Gastrointestinal safety and anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative in the rat
Abstract
Background & aims Gastrointestinal damage caused by nonsteroidal anti-inflammatory drugs (NSAIDs) remains a significant clinical problem. Hydrogen makes an important contribution to mucosal defense, and NSAIDs can suppress its synthesis. In this study, we evaluated the gastrointestinal safety and anti-inflammatory effects of a novel "HS-NSAID" (ATB-337) that consists of diclofenac linked to a hydrogen sulfide-releasing moiety.Methods The gastrointestinal injury-inducing effects of single or repeated administration of diclofenac versus ATB-337 were compared in rats, as were their effects on prostaglandin synthesis and cyclooxygenase-1 and -2 activities. The ability of these drugs to reduce carrageenan-induced paw edema and to elicit leukocyte adherence to the vascular endothelium (intravital microscopy) were also examined in rats.Results Diclofenac (10-50 micromol/kg) dose-dependently damaged the stomach, while ATB-337 did not. Repeated administration of diclofenac caused extensive small intestinal damage and reduced hematocrit by 50%. ATB-337 induced >90% less intestinal damage and had no effect on hematocrit. Diclofenac, but not ATB-337, elevated gastric granulocyte infiltration and expression of tumor necrosis factor alpha, lymphocyte function-associated antigen 1, and intercellular adhesion molecule 1. ATB-337 inhibited cycloxygenase-1 and cyclooxygenase-2 activity as effectively as diclofenac. ATB-337 did not induce leukocyte adherence, whereas diclofenac did, and was more potent at reducing paw edema.Conclusions An HS-NSAID spares the gastric mucosa of injury despite markedly suppressing prostaglandin synthesis. This effect may be related to hydrogen sulfide-mediated inhibition of tumor necrosis factor-alpha expression and of the leukocyte adherence to vascular endothelium normally induced by cyclooxygenase inhibitors.
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Suppression of endogenous H2S synthesis impairs gastric and colonic mucosal defence, and impairs healing of ulcers.
“Suppression of endogenous H2S synthesis has been shown to impair gastric and colonic mucosal defence, and to impair healing of ulcers [26], [27], [34], [35].”
From Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis (2014) · cites this paper as [26]
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- Authors
- Wallace, J. L., Caliendo, G., Santagada, V., Cirino, G., & Fiorucci, S.
- Affiliations
- University of Calgary (CA)
- University of Naples Federico II (IT)
- Corresponding author
- Wallace, John L.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2007-01
- Volume
- 132
- Issue
- 1
- Pages
- 261-271
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W2163895651
- Cited by
- 271
- References
- 39
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 6 · 2023: 9 · 2022: 13 · 2021: 13 · 2020: 12 · 2019: 13 · 2018: 9 · 2017: 23 · 2016: 19 · 2015: 26 · 2014: 23 · 2013: 22 · 2012: 18
- FWCI
- 6.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Health Sciences › Medicine › Surgery › Hydrogen's biological and therapeutic effects
- Keywords
- diclofenac, NSAID-induced gastrointestinal injury, gastroprotection, cyclooxygenase-1, cyclooxygenase-2, prostaglandin synthesis, TNF-α, leukocyte adhesion, paw edema, small bowel injury, hematocrit, anti-inflammatory activity
- MeSH terms
- Animals, Anti-Inflammatory Agents, Non-Steroidal, Blood Platelets, Diclofenac, Gastric Acid, Heterocyclic Compounds, 1-Ring, Humans, Hydrogen Sulfide, Male, Platelet Aggregation Inhibitors, Stomach, Drug Design, Cyclooxygenase Inhibitors, Rats, Wistar, Rats, Cyclooxygenase 1, Cyclooxygenase 2
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