Indomethacin-induced gastric injury and leukocyte adherence in arthritic versus healthy rats☆
References (30)
- et al.
A monoclonal antibody against the CD18 leukocyte adhesion molecule prevents indomethacin-induced gastric damage in rabbits
Gastroenterology
(1991) - et al.
Modulation of leukocyte adhesion in rat mesenteric venules by aspirin and salicylate
Gastroenterology
(1992) - et al.
Toward an epidemiology of gastropathy associated with non-steroidal antiinflammatory drug use
Gastroenterology
(1989) - et al.
Effect of aspirin plus hydrochloric acid on the gastric mucosal microcirculation
Gastroenterology
(1987) - et al.
Determination of some anti-inflammatory drugs in serum by HPLC
J Chromatogr
(1979) - et al.
Pathogenesis of NSAID-gastropathy: are neutrophils the culprits?
Trends Pharmacol Sci
(1992) - et al.
A major portion of polymorphonuclear leukocyte and T lymphocyte migration to arthritic joints in the rat is LFA-1/MAC-1-independent mechanisms
Clin Immunol Immunopathol
(1993) - et al.
Prostaglandin E2 regulates macrophage-derived tumor necrosis factor gene expression
J Biol Chem
(1988) - et al.
Regulation of macrophage tumour necrosis factor production by prostaglandin E2
Biochem Biophys Res Commun
(1986) - et al.
Effect of indomethacin on the kinetics of tumour necrosis factor alpha release and tumour necrosis factor alpha gene expression by human blood monocytes
Pharmacol Res
(1991)
Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
Nature New Biol
Gastric ulceration induced by nonsteroidal anti-inflammatory drugs is a neutrophil dependent process
Am J Physiol
Aspirin-induced acute gastric mucosal injury is a neutrophil-dependent process in rats
Am J Physiol
Role of endothelial adhesion molecules in NSAID-induced gastric mucosal injury
Am J Physiol
Indomethacin-induced leukocyte adhesion in mesenteric venules: role of lipoxygenase products
Am J Physiol
Cited by (111)
Diseases of the Alimentary Tract
2019, Large Animal Internal MedicineThe effect of 1,25 dihydroxyvitamin D3 on HCl/Ethanol-induced gastric injury in rats
2018, Tissue and CellCitation Excerpt :In this study, we also evaluated the role of participation of PGs, non-protein SH groups, and KATP channels in the gastroprotective effect of 1,25 dihydroxyvitamin D3 against HCl/Ethanol-induced gastric injury. The absence of PGs may cause decrement in mucus and bicarbonate secretion, increment in acid secretion, decreased gastric blood flow, and may augment neutrophil activation and infiltration leading to ROS production and lipid peroxidation (Ashley et al., 1985; Fiorucci et al., 2003; McCafferty et al., 1995; Wallace and Devchand, 2005). Non-steroidal anti-inflammatory agents, such as indomethacin, promote decrease of COX activity and production of endogenous PGs. Ethanol is a necrotizing agent that induces injury in gastric mucosa by constriction of venules and it has been shown that exogenous PGs revert this effect (Saeki et al., 2004).
Polymeric nanocapsules as a technological alternative to reduce the toxicity caused by meloxicam in mice
2016, Regulatory Toxicology and PharmacologyCitation Excerpt :A focal inflammatory infiltrate in the mucosa and submucosa of the stomach was demonstrated after M-F treatment, indicating an inflammatory process in the tissue and more pronounced damage. In fact, leukocytes have a function in NSAID-induced gastric injury, since the severity of the injury can be greatly reduced by prior induction of neutropenia (McCafferty et al., 1995). The most common side effects of meloxicam are gastrointestinal irritation, but toxic effects have been demonstrated in liver (Hargus et al., 1995; Vane and Botting, 1997; Lapeyre-Mestre et al., 2006).
H<inf>2</inf>S-releasing drugs: Anti-inflammatory, cytoprotective and chemopreventative potential
2015, Nitric Oxide - Biology and ChemistryNesfatin-1 alleviates gastric damage via direct antioxidant mechanisms
2015, Journal of Surgical ResearchCitation Excerpt :Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most widely consumed drugs that are used to treat inflammatory pain [1], but their use is limited by formation of gastric ulcers and impairment of their healing [2]. Indomethacin is an NSAID with pain-relieving, antipyretic, and anti-inflammatory properties, which is known to produce serious side effects, causing erosions, ulcerative lesions, and petechial bleeding in the mucosa of stomach [3]. The major cause of acute gastric ulcerogenic response due to indomethacin is related with reduced prostaglandin synthesis via the inhibition of cyclooxygenase (COX), including the inhibition of both isoenzymes, COX-1, and COX-2 [4,5].
- ☆
Supported by a grant from the Medical Research Council of Canada (MRC). Dr. Wallace is an MRC Scientist and an Alberta Heritage Foundation for Medical Research (AHFMR) Scientist. Dr. McCafferty is an AHFMR Fellow.