Role of nitric oxide in pathogenesis of gastric mucosal damage induced by compound in rats

Yasuhiro, Tetsuya; Konaka, Akira; Ukawa, Hideki; Kato, Shinichi; Takeuchi, Koji

doi:10.1016/s0928-4257(97)89477-6

Cited by 25 publications

(6 citation statements)

References 19 publications

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“…Moreover, cimetidine has been found to have no preventive effect against the lesion development in both models. The increase in free radical nitric oxide (peroxynitrite) production by iNOS has also been found to be associated with the development of lesions as well [22]. In the present study, the beneficial effect of aminoguanidine against the development of lesions in both models confirms the important role of iNOS in enhancing lesion progression.…”

Section: Discussionsupporting

confidence: 81%

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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Section: Discussionsupporting

confidence: 81%

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

et al. 2006

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“…Increased mucosal iNOS, reduced cNOS, and augmented nitrite/nitrate levels in the lumen are common features of the damage induced by other deleterious agents such as NSAIDs (Piotrowski et al, 1999), mast cell degranulation (Yasuhiro et al, 1997a), serotonine (Yasuhiro et al, 1997b), or cigarette smoke (Chow et al, 1998). Inhibition of iNOS reduces the level of gastric damage in many of these experimental models of injury (Chow et al, 1998;Nishida et al, 1998b;Yasuhiro et al, 1997a,b), thus confirming the deleterious effect of the massive release of NO.…”

Section: Nitric Oxide and Gastricmentioning

confidence: 84%

Nitric oxide: Relation to integrity, injury, and healing of the gastric mucosa

Calatayud

Barrachina

Esplugues

2001

Microscopy Res & Technique

100

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Nitric oxide (NO) plays a multifaceted role in mucosal integrity. The numerous functions of NO and the double-edged role played by NO in most of them provide a great complexity to the NO action. The three enzymatic sources of NO, neuronal NO-synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), have been characterised in the gastrointestinal tract. The protective properties of the NO derived from constitutive NO-synthases (eNOS and nNOS) have already been well established. Less clear is the role assigned to iNOS. The simplistic initial view of low levels of NO synthesised by constitutive NOS being protective while exaggerated NO levels after iNOS induction leading irremediably to cytotoxicity is being questioned by new evidence. As initially reported for constitutive NOS, iNOS activity may be associated to reduced leukocyte-endothelium interaction and platelet aggregation as well as protection of mucosal microcirculation. Moreover, iNOS activity may be important to resolve inflammation by increasing apoptosis in inflammatory cells. It is entirely possible that a low level of expression of iNOS will reflect a positive host-defense response to challenge, but that exaggerated or uncontrolled expression of iNOS itself becomes detrimental. There is no doubt about the protective role of NO in physiological conditions. However, when the mucosa is threatened, the role of NO becomes multiple and the final effect will probably depend on the nature of the insult, the environment involved, and the interaction with other mediators.

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“…Although NO is considered to be important in maintaining gastric mucosal integrity, recent studies also showed a detrimental role for NO in inflammatory gastrointestinal disorders; thus some of the mechanisms that have been proposed to explain the increase in NO in other experimental studies may be operating in the gastric mucosa after NSAID administration (51)(52)(53)(54)(55).…”

Section: Figmentioning

confidence: 99%

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

2005

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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.

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Role of nitric oxide in pathogenesis of gastric mucosal damage induced by compound in rats

Cited by 25 publications

References 19 publications

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

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

Nitric oxide: Relation to integrity, injury, and healing of the gastric mucosa

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

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