Cited by 271Inflammatory mediators and NSAID effectsSulfur Compounds in BiologyHydrogen's biological and therapeutic effects

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Gastrointestinal safety and anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative in the rat

Wallace, John L., Caliendo, Giuseppe, Santagada, Vincenzo, Cirino, Giuseppe, Fiorucci, Stefano·2007·Gastroenterology

DOI 10.1053/j.gastro.2006.11.042

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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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Self-citation

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.
ORCID: Wallace, John L.
Caliendo, Giuseppe
Santagada, Vincenzo
Cirino, Giuseppe
Fiorucci, Stefano
Venue: Gastroenterology
Publisher: Elsevier BV
Published: 2007-01
Volume: 132
Issue: 1
Pages: 261-271
ISSN: 0016-5085 (ISSN-L)
DOI: 10.1053/j.gastro.2006.11.042
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Gastroenterology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › 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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Gastrointestinal safety and anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative in the rat

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