Role of polymorphonuclear leukocytes and oxygen-derived free radicals in chronic gastric lesion induced by acetic acid in rat

Motilva, Virginia; Martín, Maria J.; Luque, M.I.; Lastra, Catalina Alarcón de la

doi:10.1016/0306-3623(95)02025-x

Cited by 25 publications

(10 citation statements)

References 26 publications

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“…The circulating neutrophils play a critical role in the pathogenesis of NSAID (Wallace et al, 1990) and acetic acid mucosal lesions (Motilva et al, 1996). Neutrophils might contribute to gastric ul ceration by several possible mechanisms such as production of reactive oxygen metabolites, release of proteases and lipid mediators, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…In the same way, various anti oxidant enzymes such as superoxide dismutase (SO D ), an important radical superoxide scaven ger, and glutathione peroxidase (GSH-Px), an en zyme involved in the elimination of hydrogen per oxide and lipid hydroperoxides, play an important role in cell protection. Recently, the role of neu trophils has been proposed in the gastric lesions induced by NSAIDs (Wallace et al, 1990), acetic acid (Motilva et al, 1996) or ethanol (Kvietys et al, 1990). These leukocytes adhere to endothelial cells, thereby blocking capillaries and damaging the endothelial integrity through the release of proteases, leukotrienes and active oxidants (Jacob son, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

Martín

Lacasa

Alarcón‐de‐la‐Lastra

et al. 1998

Zeitschrift Für Naturforschung C

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The anti-ulcerogenic and anti-oxidant effects of various flavonoids have been frequently reported. We investigated the cytoprotective properties of quercetin, a natural flavone, in gastric mucosal injury induced by 50% ethanol, since in this experimental model the patho genesis of the lesions has been related with production of reactive oxygen species. The in volvement of neutrophil infiltration and the capacity of this flavonoid to restrain the oxida tive process produced in the gastric tissue after ethanol administration were also investigated. Oral pretreatment with the highest dose of quercetin (200 mg/kg), 120 min before absolute ethanol was the most effective anti-ulcer treatment. Thiobarbituric acid reactive substances in the gastric mucosa, an index of lipid peroxidation, were increased by ethanol injury, but the increase was inhibited by the administration of 200 mg/kg of quercetin. This dose also induced a significant enhancement in the levels of mucosal non-protein SH compounds (im portant anti-oxidant agents) and in glutathione peroxidase activity. Exposure of the gastric mucosa to 50% ethanol induced a significant increase in myeloperoxidase activity, an index of neutrophil infiltration. Flowever, quercetin was not able to modify the increase in enzy matic activity generated by the necrotizing agent. The activity of superoxide dismutase en zyme involved in several antioxidant processes was also not significantly modified after quer cetin treatment.These results suggest that the anti-ulcer activity of quercetin in this experimental model could be partly explained by the inhibition of lipid peroxidation, through decrease of reactive oxygen metabolites. However, the inhibition of neutrophil infiltration or the increase of su peroxide dismutase activity does not appear to be involved in gastroprotective effect of this flavonoid.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

Martín

Lacasa

Alarcón‐de‐la‐Lastra

et al. 1998

Zeitschrift Für Naturforschung C

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“…Motilva et al 136) examined the role of oxygen-derived free radicals by measuring MPO as an index of leukocyte infiltration. MPO activity was significantly increased 7 and 14 d after acetic acid ulcer induction.…”

Section: Miscellaneous Drugs and Endogenous Sub-mentioning

confidence: 99%

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Okabe

Amagase

2005

Biological & Pharmaceutical Bulletin

208

166

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Four types of experimental chronic ulcer models, named acetic acid ulcer models, have been developed to examine the healing process of peptic ulcers, screen anti-ulcer drugs, and better evaluate the adverse effects of various anti-inflammatory drugs on the gastrointestinal mucosa. The model easily and reliably produces round, deep ulcers in the stomach and duodenum, allowing acetic acid ulcer production in mice, rats, Mongolian gerbils, guinea pigs, cats, dogs, miniature pigs, and monkeys. These ulcer models highly resemble human ulcers in terms of both pathological features and healing process. The models have been established over the past 35 years and are now used throughout the world by basic and clinical scientists. One of the characteristic features of acetic acid ulcers in rats is the spontaneous relapse of healed ulcers Ͼ100 d after ulceration, an endoscopically confirmed phenomenon. Indomethacin significantly delays the healing of acetic acid ulcers, probably by reducing endogenous prostaglandins and inhibiting angiogenesis in ulcerated tissue. Helicobacter pylori significantly delays healing of acetic acid ulcers and causes relapse of healed ulcers at a high incidence in Mongolian gerbils. Anti-secretory drugs (e.g. omeprazole), prostaglandin analogs, mucosal defense agents (e.g. sucralfate), and various growth factors all significantly enhance healing of acetic acid ulcers. Gene therapy with epidermal growth factor and vascular endothelial growth factor applied to the base of acetic acid ulcers in rats is effective in enhancing ulcer healing. Since an inhibitor of nitric oxide syntase prevents ulcer healing, nitric oxide might be involved in the mechanism underlying ulcer healing. We conclude that acetic acid ulcer models are quite useful for various studies related to peptic ulcers.

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“…It has been suggested that the proliferation of mucosal cells, neovascularization, adequate mucosal blood flow, and growth factors such as transforming growth factor or epidermal growth factor contribute to the healing process of the produced ulcer [11,23]. Recently, oxygen free radicals derived from infiltrated neutrophil have been found to exert an inhibitory effect on the healing of ulcers, and it has been found that the reduction of neutrophil infiltration into ulcerated tissues or the inhibition of enhanced lipid peroxidation in ulcerated tissues promotes the ulcer healing process [24]. In the present study, both cimetidine and aminoguanidine were found to possess the significant healing-promoting effect on acetic acid-induced chronic gastric ulcer, suggesting the role of overproduction of nitric oxide by iNOS of activated macrophage in the development of ulcer and the involvement of gastric acid in aggravating gastric ulcer.…”

Section: Discussionmentioning

confidence: 98%

Preventive and curative effects of curcumin on the development of gastric inflammatory diseases in rats

et al. 2006

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Preventive and curative effects of curcumin on experimental acute and chronic gastric ulcers were investigated to validate its clinical application on a remedy for peptic ulcer. Intraduodenal administration of curcumin, 5-20 mg/kg, inhibited gastric acid secretion in pylorus-ligated rats, and oral administration prevented ethanol-induced acute gastric mucosal lesions. Curcumin (20-80 mg/kg, p.o.) dose-dependently prevented both serotonin-induced gastric mucosal lesions and compound 48/80-induced gastric mucosal lesions in rats. Furthermore, oral administration of curcumin, 10-80 mg/kg, twice daily for 10 days, significantly accelerated the healing of acetic acid-induced chronic gastric ulcer and promoted mucosal regeneration in the ulcerated portion in a dose-related manner. Cimetidine prevented the formation of ethanol-induced gastric mucosal lesions, but not of serotonin-induced and compound 48/80-induced gastric mucosal lesions. Consecutive administration of cimetidine showed a marked acceleration in the healing of acetic acid-induced ulcer. Aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, showed anti-ulcerogenic effects similar to those oberved for curcumin. The present results indicate that curcumin exhibits gastric cytoprotection in the acute lesion models and ulcer healing promotion in the chronic ulcer model. The preventive and curative effects of curcumin might be due to an increase in the mucosal defensive mechanism through its antioxidant property and inhibition of NO or cytokine-mediated inflammation.

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Role of polymorphonuclear leukocytes and oxygen-derived free radicals in chronic gastric lesion induced by acetic acid in rat

Cited by 25 publications

References 26 publications

Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Preventive and curative effects of curcumin on the development of gastric inflammatory diseases in rats

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Role of polymorphonuclear leukocytes and oxygen-derived free radicals in chronic gastric lesion induced by acetic acid in rat

Cited by 25 publications

References 26 publications

Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

Anti-Oxidant Mechanisms Involved in Gastroprotective Effects of Quercetin

An Overview of Acetic Acid Ulcer Models<br>&mdash;The History and State of the Art of Peptic Ulcer Research&mdash;

Preventive and curative effects of curcumin on the development of gastric inflammatory diseases in rats

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An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—