Nitric oxide mechanisms in protection afforded by L-arginine in ibuprofen induced gastric toxicity

Jimenez, Dolores; Pozo, David; Lastra, Catalina Alarcón de la; Esteban, J.; Leo, Bruseghini; Esteras, Antonio; Herrerias, Juan Manuel; Martín, Maria J.; Motilva, Virginia

doi:10.1016/s0016-5085(00)80853-7

Cited by 10 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study shows that co-administration of arginine with ibuprofen prevented ibuprofen-induced gastric mucosal injury (30). The authors also suggest that arginine may protect against ibuprofen-induced gastric mucosal injury by the inhibition of nitric oxide synthase activity.…”

Section: Discussionmentioning

confidence: 96%

“…Group 1: To eight rats ibuprofen (purchased from Sigma Chemical Co., St. Louis, Missouri, USA) was administered at a concentration of 100 mg/kg body weight in 5% sodium bicarbonate by gavage (30). Group 2: To eight rats N G -arginine methyl ester (Sigma) dissolved in distilled water was administered by gavage at the concentration of 30 mg/kg body weight (31) 1 hr before the administration of ibuprofen.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Nitro-Arginine Methyl Ester, a Non-Selective Inhibitor of Nitric Oxide Synthase Reduces Ibuprofen-Induced Gastric Mucosal Injury in the Rat

2005

View full text Add to dashboard Cite

Ibuprofen is a commonly used non-steroidal anti-inflammatory drug. Gastrointestinal adverse drug reactions from ibuprofen usage include gastric mucosal ulcers and bleeding. The mechanism by which ibuprofen induces gastric mucosal damage is not clear. The present study is an attempt to examine the role of nitric oxide in the pathogenesis of ibuprofen-induced gastric mucosal damage. Ibuprofen administered orally at the dose of 100 mg/kg body weight for 6 days to the rats resulted in gastric mucosal injury. Serum nitrite and nitrosothiol were increased significantly as compared with the controls, which were treated with the vehicle alone. In the gastric mucosa, lipid peroxidation and protein thiols were increased, and the activity of glyceraldehyde 3-phosphate dehydrogenase, a nitric oxide sensitive enzyme was decreased significantly. Pretreatment of the rats daily with nitric oxide synthase inhibitor, nitro-arginine methyl ester (30 mg/kg body weight) 1 hr before treatment with ibuprofen reduced the gastric mucosal injury. Biochemically, it prevented the rise in serum nitrite levels and the increase in lipid peroxidation and protein thiol levels and the loss of glyceraldehyde 3-phosphate dehydrogenase activity in the gastric mucosa. The results of the present study suggest that increased nitric oxide production may be one of the mechanisms by which ibuprofen produces gastric mucosal injury and that inhibition of nitric oxide synthase reduces gastric mucosal injury.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Nitro-Arginine Methyl Ester, a Non-Selective Inhibitor of Nitric Oxide Synthase Reduces Ibuprofen-Induced Gastric Mucosal Injury in the Rat

2005

View full text Add to dashboard Cite

show abstract

“…However, adequate concentrations are related to the homeostatic control of the mucosa due to the interaction with protective molecules, such as endogenous PGs. The decrease in the endothelial isoform (eNOS) is related to the increase in tissue damage [51][52][53].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Modulates the Effects of Gastric Injury in Rats: Role of Prostaglandins and Nitric Oxide

Deogracias¹,

Alarcón‐de‐la‐Lastra²,

Jimenez³

et al. 2003

Neurosignals

Self Cite

View full text Add to dashboard Cite

Experimental evidence has been presented connecting melatonin with the prevention or treatment of gastrointestinal disorders either by the scavenging properties of active oxygen or by receptor-mediated stimulation of gene expression of neutralizing enzymes. Prostaglandins and nitric oxide are important neuroimmunomodulators in digestive physiology and different studies have indicated that the protective properties of melatonin may be explained by prostaglandin and/or nitric oxide mechanisms. The aim of the present study was to examine the effect of intraperitoneal administration of melatonin on in vivo changes in PGE₂, generated in gastric mucosal lesions by ischemia-reperfusion. Cyclic GMP nucleotide was also studied as an index of the principal enzymatic activity involved in the metabolism of nitric oxide, the nitric oxide synthase. The different immunological tests showed that the intraperitoneal administration of melatonin prevents the postischemic decrease in prostaglandins. The concentration of this eicosanoid in the rat mucosa treated with 20 mg·kg^–1 of melatonin was significantly higher (p < 0.05) than that in the control rats. The amount of cyclic GMP in the stomach decreased because of ischemia-reperfusion. In treated animals however, a marked increase occurred in concentrations of GMP, but the difference was not statistically significant. The results suggest that the mechanism of protection afforded by melatonin against lesions induced by gastric ischemia-reperfusion may be due to stimulation of the synthesis of eicosanoid protectors during the ischemic process.

show abstract

“…Some studies have suggested that the release of NO could revert the gastric alterations provoked by NSAID and lower the gastric toxicity of NO-releasing NSAIDs [9,10] by activating cGMPdependent pathways [11]. However, overproduction of NO due to expression of the inducible isoforms of NOS (iNOS) also has been implicated in inflammatory gastrointestinal disorders [12,13]. In this way, NO shows a dual behaviour: at physiological concentrations, released through the cNOS, it regulates house-keeping functions, whereas its overproduction by the iNOS exhibits cytotoxic activity because interacting with reactive species producing peroxinitrites and other compounds, which are highly damaging for the tissues.…”

Section: Introductionmentioning

confidence: 99%

Role of prostaglandins and nitric oxide in gastric damage induced by metamizol in rats

et al. 2002

View full text Add to dashboard Cite

show abstract

Nitric oxide mechanisms in protection afforded by L-arginine in ibuprofen induced gastric toxicity

Cited by 10 publications

References 0 publications

Nitro-Arginine Methyl Ester, a Non-Selective Inhibitor of Nitric Oxide Synthase Reduces Ibuprofen-Induced Gastric Mucosal Injury in the Rat

Nitro-Arginine Methyl Ester, a Non-Selective Inhibitor of Nitric Oxide Synthase Reduces Ibuprofen-Induced Gastric Mucosal Injury in the Rat

Melatonin Modulates the Effects of Gastric Injury in Rats: Role of Prostaglandins and Nitric Oxide

Role of prostaglandins and nitric oxide in gastric damage induced by metamizol in rats

Contact Info

Product

Resources

About