Cyclosporin A Reduces the Severity of Cold-Restraint-Induced Gastric Lesions: Role of Leukocytes

Coşkun, Tamer; Ali̇can, İnci̇; Yeğen, Berrak Ç.; Şan, Tangül; Çetınel, Şule; Kurtel, Hızır

doi:10.1159/000201246

Cited by 8 publications

(9 citation statements)

References 18 publications

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“…In vivo research in the cat mesentery, hamster skin, and rat ear showed that hypoperfusion during ischemia enhanced the adhesion of leukocytes to the vascular endothelium [6,22]. Polymorphonuclear leukocytes (PMNs) have been implicated in the pathogenesis of stress ulcers by many investigators [23,24]. We observed that inhibition of NO synthesis increased PMN infiltration and enhanced gastric mucosal dysfunction in hemorrhagic stress-induced ulcers.…”

Section: Discussionmentioning

confidence: 78%

Role of Nitric Oxide in Gastric Injury Induced by Hemorrhagic Shock in Rats

Denizbaşı

Yeğen²,

Öztürk³

et al. 2000

Pharmacology

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The aim of this study was to investigate the effect of nitric oxide (NO) on the gastric injury induced by hemorrhagic shock. Hemorrhagic shock was created by withdrawing 3 ml blood/200 g body weight of the rats. Before the hemorrhage, N^G-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus), D-NAME (10 mg/kg i.v. bolus), or L-arginine (100 mg/kg i.v. bolus and 10 mg/kg/min infusion) + L-NAME were administered. At the end of the 1-hour hypovolemic shock period, histological analysis, gastric ulcer index, gastric myeloperoxidase (MPO) activity, and gastric protein oxidation (PO) levels were determined. In histological analysis a destructive effect of L-NAME (NO synthase inhibitor) was demonstrated. L-NAME treatment increased gastric MPO activity, L-arginine reversed this effect and D-NAME had no effect. Tissue PO activity was found to be increased in L-NAME-treated rats; L-arginine treatment reversed this activity. It is concluded that gastric barrier function is altered after hemorrhagic shock, and L-arginine (NO precursor) can prevent mucosal injury in the stomach. This effect of NO may be on gastric blood flow and can be mediated by tissue neutrophils.

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Section: Discussionmentioning

confidence: 78%

Role of Nitric Oxide in Gastric Injury Induced by Hemorrhagic Shock in Rats

Denizbaşı

Yeğen²,

Öztürk³

et al. 2000

Pharmacology

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“…The stress ulcer model stimulates the production of oxygen-derived free radicals (in endothelial cells and polymorphonuclear neutrophiles) which cause gastric mucosal tissue damage by inducing ischemia at the level of gastric microvasculature, and the direct role of the oxygen free radicals in the etiopathology of acute stress ulcers has been established (Coskun et al 1995, Ohara et al 1990Manicelli et al 1990). It is well known that the exposure of gastric mucosa to damaging factors such as water immersion/restraint stress and NSAIDs produce acute ulcers that are mainly mediated by ROS (Carnevale et al 2011), and gastric protection against absolute ethanol injury in rats has been linked to antioxidant activity (de-Faria et al 2012) .…”

Section: Discussionmentioning

confidence: 99%

“…Following 12 hours of food (but not water) deprivation, test rats were given the extract (100 and 200 mg/kg) by oral route while control rats received the vehicle. One hour later, the rats were placed in small individual wire cages and immersed in cold water (3)(4)(5) o C), up to the level of the xiphoid. 120, minutes later blood samples were taken and the animals were sacrificed using ether and the stomachs removed for the assessment of lesion formation and mucus production (lesion indices expressed as the sum of the lengths of the lesions for each rat).…”

Section: Cold Stress-induced Gastric Lesionsmentioning

confidence: 99%

Cytoprotective and antioxidant effects of the methanol extract of <i>Eremomastax Speciosa</i> in rats

Amang¹,

Tan²,

Patamaken³

et al. 2013

Afr. J. Trad. Compl. Alt. Med.

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Background: Ethno-botanical information shows that Eremomastax speciosa is used in the traditional management of various stomach complaints including gastro-duodenal ulcers. Materials and Methods:In this study, we tested the cytoprotective potential of the whole plant methanol extract (100-200 mg/kg, p.o), against HCl/ethanol, absolute ethanol, cold/restraint stress rats, and pylorus legated rats pre-treated with indomethacin. The effects of the extract on gastric lesion inhibition, the volume of gastric juice, gastric pH, gastric acid output, mucus production and gastric peptic activity were recorded. Oxidative stress parameters were measured in blood and gastric tissue samples obtained from the animals in all the models tested. Results: The extract significantly (p<0.05), reduced the formation of cold/restraint ulcers by (31-60%, inhibition), completely inhibited (100%) the formation of lesions induced by HCl/ethanol at the highest dose, but was less effective against absolute ethanol (22-46% inhibition). The extract (200 mg/kg), significantly reduced lesion formation (P<0.01), gastric acidity (P<0.01), and volume of gastric secretions (P<0.05), in the indomethacin/pylorus ligation model, and did not affect the activity of pepsin in gastric juice. Blood concentrations of antioxidant enzymes (catalase, SOD and GSH), increased significantly and MDA concentrations decreased in all models tested. Conclusion: Cytoprotection by E. speciosa methanol extract was attributed to its ability to reduce acid secretion, and to enhance mucosal defence and in vivo antioxidant status.

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“…Recent studies suggest that toxic oxygen molecules might be one of the important factors in inducing gastric mucosal injury during cold‐restraint stress and the increase of xanthine oxidase activity might be responsible for the production of oxygen free radicals. 1,2,15 Lipid peroxidation, which results from the generation of reactive oxygen species, was suggested to be closely related to production of the gastric damage by cold‐restraint stress.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies suggest that oxygen free radicals might be one of the important factors in inducing gastric mucosal injury during stress. 1,2,15…”

mentioning

confidence: 99%

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Tunçel

Erkasap

Şahıntürk

et al. 1998

Annals of the New York Academy of Sciences

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The pathogenesis of cold-restraint stress ulcer involves various factors and is not completely understood. Mast cell degranulation, increased gastric muscular contractility, diminished mucosal blood flow, release of several biogenic amines, activated polymorphonuclear leukocytes, and lipid peroxidation which results from toxic oxygen molecules were suggested to be related to the production of gastric damage by cold-restraint stress. Recent evidence strongly indicates that VIP has a modulatory effect on tissue injury. Sprague-Dawley rats were used in two series of experiments. One set of rats was exposed to cold-restraint stress with some of the rats pretreated with VIP. The second set of rats was exposed to cold-restraint stress and then was administered VIP for different durations. Cold-restraint stress induced gastric lesions and mast cell degranulation and also increased lipid peroxidation in gastric tissue. VIP prevented stress-induced ulcers and mast cell degranulation and protected gastric tissue from lipid peroxidation. When VIP was used after induction of stress ulcer it was therapeutically beneficial. Thanks to its antioxidant and anti-inflammatory activity, VIP can be valuable in the prevention of gastric mucosal damage induced by cold-restraint stress.

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Cyclosporin A Reduces the Severity of Cold-Restraint-Induced Gastric Lesions: Role of Leukocytes

Cited by 8 publications

References 18 publications

Role of Nitric Oxide in Gastric Injury Induced by Hemorrhagic Shock in Rats

Role of Nitric Oxide in Gastric Injury Induced by Hemorrhagic Shock in Rats

Cytoprotective and antioxidant effects of the methanol extract of <i>Eremomastax Speciosa</i> in rats

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

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