Contribution of NO synthases to neutrophil infiltration in the gastric mucosal lesions in rats with water immersion restraint stress

Nishida, Keiji; Ohta, Yoshiji; Ishiguro, Isao

doi:10.1016/s0014-5793(98)00237-3

Cited by 56 publications

(52 citation statements)

References 40 publications

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“…In addition, NO from cNOS has an inhibitory role in neutrophil-endothelial cell adhesive interactions in postcapillary venules, leading to the inhibition of neutrophil infiltration into tissues (Nishida et al, 1999). Similar results obtained in other reports also indicated that a decrease in cNOS could contribute to an increase in neutrophil infiltration in the gastric mucosa of water immersion restraint (WIR)-stressed rats, which may help to maintain the mucosal integrity of the stomach (Nishida et al, 1998). However, NO generated by iNOS may be involved in leukocyte adhesion, inflammatory cell infiltration and parenchyma cell dysfunction (Kobata et al, 2007;Lanteri et al, 2003), all have a deleterious influence on the gastric mucosal integrity.…”

Section: Discussionsupporting

confidence: 76%

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Liu

Gou

et al. 2013

Pharmaceutical Biology

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Context: Rutin, a flavonoid commonly present in onions, apples and tea, has been suggested to have a variety of pharmacological activities, including immunomodulator, anti-inflammatory and antioxidant activities. Objectives: The present study was to examine the protective effects of rutin on gastric mucosal damage induced by gastric ischemia-reperfusion (I/R) in rats. Materials and methods: Rutin (50, 100, 200 mg/kg) was administered intragastrically for five consecutive days before ischemia. Sixty minutes after the last administration of rutin, under anesthesia, the celiac artery was clamped for 30 min, and then the clamp was removed for 60 min reperfusion. After reperfusion, the stomach was removed for biochemical and histological examinations. Results: As compared with the I/R group (116.7 AE 21.5), administration of rutin at doses of 50, 100 and 200 mg/kg significantly prevented the increase of gastric mucosal injury index induced by gastric I/R (73.4 AE 14.8, 65.9 AE 9.6 and 26.9 AE 5.7, respectively). ED 50 value was 138.7 mg/kg. Moreover, rutin at doses of 50, 100 and 200 mg/kg showed an inhibition on the increased myeloperoxidase (24.6, 41.3 and 53.1% reduction) activity and malondialdehyde levels (27.4, 40.3 and 50.7% reduction) in gastric mucosa. Also, the elevation of inducible NO synthase (iNOS) activity as well as the decrease of constitutive NO synthase (cNOS) in the gastric mucosa were significantly prevented by rutin pretreatment. Conclusion: These results suggested that rutin has a protective effect against gastric mucosal injury induced by gastric I/R and that the gastroprotection was related to the NOS/NO pathway and its antioxidant activity.

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Section: Discussionsupporting

confidence: 76%

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Liu

Gou

et al. 2013

Pharmaceutical Biology

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“…Neutrophil infiltration plays a very important role in the progression of injury and inflammation by aggregation and release of tissue-disrupting substance in various tissues, plus gastric mucosal lesions [26,27]. Prior study has established that neutrophil infiltration into gastric mucosal tissues is involved in the progress of acute gastric mucosal lesions [28]. The accumulation of neutrophil infiltration into the gastric mucosal tissues is estimated by MPO [29].…”

Section: Discussionmentioning

confidence: 99%

Assessment of Gastroprotective Potential of <i>Delonix regia</i> (Boj Ex Hook) Raf against Ethanol and Cold Restrain Stress-Induced Ulcer in Rats

Sachan¹,

Chandra²,

Pal³

2015

Trop. J. Pharm Res

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“…Recruitment and activation of neutrophils contribute greatly to the pathophysiological processes occurring in gastric mucosa at the later stage of stress (13,14). Synthesis and release of inflammatory mediators, especially of proinflammatory cytokines such as TNF-␣, IL-1␤, and IL-18, of chemokines such as cytokine-induced neutrophil chemoattractant-1 (CINC-1, a rat analog of human IL-8/Gro-␣ and a potent neutrophil chemoattractant), and of adhesion molecules such as ICAM-1 as well as of inducible NO synthase/NO, are recently emerged as important determinants of mucosal inflammation and gastric injury following cold immobilization stress (15)(16)(17)(18)(19)(20). However, despite intense research, much is unknown about the molecular mechanism or the signal transduction mechanism by which this type of stress induces the incidence of acute gastric mucosal injury.…”

mentioning

confidence: 99%

Activation of p38 MAPK by Reactive Oxygen Species Is Essential in a Rat Model of Stress-Induced Gastric Mucosal Injury

Jia

Wei

et al. 2007

The Journal of Immunology

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Stress ulceration is a common complication in critically ill patients and can result in significant upper gastrointestinal bleeding associated with a high morbidity and mortality. At present, little is known of the molecular mechanisms underlying the incidence of this type of gastric damage. In the present study, we investigated the temporal activation of the redox-sensitive p38 signaling transduction cascade and its roles in a well-defined experimental model of cold immobilization stress-induced gastric ulceration. Exposure of Sprague-Dawley rats to 6 h of cold immobilization stress led to a rapid activation of p38 in the gastric mucosa at as early as 15 min after stress, and this activation was maximal after 1.5 h of stress and still persisted until the end of stress. Selectively blocking p38 by pretreatment with SB 239063, a potent and selective p38 inhibitor, suppressed the stress-promoted TNF-α, IL-1β, and CINC-1 production and then prevented the subsequent neutrophil infiltration, gastric mucosal epithelial necrosis and apoptosis, and the ulcerative lesions formation. Prior administration of the free radical scavengers, tempol and N-acetyl-l-cysteine, abolished the stress induction of p38 activation and the resulting mucosal inflammation and gastric injury. These results demonstrate that reactive oxygen species-mediated p38 activation plays an essential role in the pathogenesis of stress-induced gastric inflammatory damage in the rat model of cold immobilization stress. Our findings suggested that inhibition of p38 activation might be a potential strategy for the prophylaxis and treatment of stress ulceration.

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Contribution of NO synthases to neutrophil infiltration in the gastric mucosal lesions in rats with water immersion restraint stress

Cited by 56 publications

References 40 publications

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Assessment of Gastroprotective Potential of <i>Delonix regia</i> (Boj Ex Hook) Raf against Ethanol and Cold Restrain Stress-Induced Ulcer in Rats

Activation of p38 MAPK by Reactive Oxygen Species Is Essential in a Rat Model of Stress-Induced Gastric Mucosal Injury

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