ArticleWorld journal of gastroenterology2008
Irsogladine maleate suppresses indomethacin-induced elevation of proinflammatory cytokines and gastric injury in rats.
Article in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Propolis and Its Gastroprotective Effects on NSAID-Induced Gastric Ulcer Disease: A Systematic Review.Nutrients · 2021Pooled it
- Freshwater Clam Extract Attenuates Indomethacin-Induced Gastric Damage In Vitro and In Vivo.Foods (Basel, Switzerland) · 2022Article
- Inhibition of GKN2 Attenuates Acute Gastric Lesions Through the NLRP3 Inflammasome.Advances in wound care · 2020Article
- Induction of COX-1, suppression of COX-2 and pro-inflammatory cytokines gene expression by moringa leaves and its aqueous extract in aspirin-induced gastric ulcer rats.Molecular biology reports · 2019Article
- Protective effects of Weilikang decoction on gastric ulcers and possible mechanisms.Journal of natural medicines · 2016Article
- The caspase-1 inhibitor AC-YVAD-CMK attenuates acute gastric injury in mice: involvement of silencing NLRP3 inflammasome activities.Scientific reports · 2016Article
- The protective effect of aged garlic extract on nonsteroidal anti-inflammatory drug-induced gastric inflammations in male albino rats.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- A sulfated-polysaccharide fraction from seaweed Gracilaria birdiae prevents naproxen-induced gastrointestinal damage in rats.Marine drugs · 2012Article
- Inhibitory Effects of ECQ on Indomethacin-Induced Gastric Damage in Rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
- Irsogladine maleate ameliorates inflammation and fibrosis in mice with chronic colitis induced by dextran sulfate sodium.Medical molecular morphology · 2012Article
- Comparison of Indomethacin, Diclofenac and Aspirin-Induced Gastric Damage according to Age in Rats.Gut and liver · 2012Article
- Present status and strategy of NSAIDs-induced small bowel injury.Journal of gastroenterology · 2009Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the mucosal protective effect and the mechanisms of action of the anti-ulcer drug irsogladine maleate in gastric injury induced by indomethacin in rats.
methodsGastric mucosal injury was induced in male Hos:Donryu rats by oral administration of indomethacin at a dose of 48 mg/kg. One hour before indomethacin treatment, animals were orally pretreated with irsogladine maleate at doses of 1 mg/kg, 3 mg/kg or 10 mg/kg. Four hours after indomethacin administration, the animals were sacrificed and their stomachs were rapidly removed and processed for the evaluation of gastric mucosal damage and the determination of the concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-8 and myeloperoxidase (MPO) in mucosal tissues.
resultsLinear hemorrhagic mucosal lesions were observed primarily in the glandular stomach 4 h after oral administration of indomethacin. Pretreatment with irsogladine maleate markedly reduced the number and severity of these lesions in a dose-dependent manner. The mucosal concentrations of proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-8) and MPO, which indicates the degree of mucosal infiltration by neutrophils, increased concomitantly with the occurrence of gastric injury in the indomethacin-treated rats. Pretreatment with irsogladine maleate significantly decreased the levels of these inflammatory factors in gastric tissue elicited by indomethacin.
conclusionThe mucosal protective effects afforded by irsogladine maleate on gastric injury induced by indomethacin are mediated by inhibition of mucosal proinflammatory cytokine production and neutrophil infiltration, leading to suppression of mucosal inflammation and subsequent tissue destruction.
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