Protective effect of a cysteine prodrug and antioxidant, L-2-oxothiazolidine-4-carboxylate, against ethanol-induced gastric lesions in rats

Moutaery, Meshal Al; Rayes, Hannan Al; Swailam, Ramaiz Al; Elfaki, Ibrahim; Khan, Haseeb A.; Arshaduddin, Mohammad; Tariq, Mohammad

doi:10.1016/j.etp.2010.08.012

Cited by 18 publications

(9 citation statements)

References 52 publications

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“…More importantly, they also protect mucus by preventing rupture of the disulfide bridges that join the mucus subunits and maintain its structural integrity. The decrease in endogenous thiol in ethanol-induced gastric injury and its role in mucosal protection have been demonstrated earlier (Al-Howiriny et al, 2010;Al Moutaery et al, 2012;Bertrand et al, 1999;Hernandez-Munoz et al, 2000). Both pre and post-treatment with zinc provided nearly similar and significant suppression of the oxidative damages to the biomacromolecules (Fig.…”

Section: Discussionmentioning

confidence: 63%

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Ineu

Oliveira

et al. 2013

Food and Chemical Toxicology

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The aim of the present study was to evaluate the possible effects of zinc chloride against the gastrointestinal lesions caused by oral administration of ethanol in rats. Rats were divided into five groups, namely, saline, ethanol, zn, zn+ethanol and ethanol+zn. Ethanol 70% (2 mL/kg) was administered by gavage in 36 h fasted rats. Zinc chloride (27 mg/kg, ~13 mg/kg of zinc) was given by gavage 1h before or 1h after the administration of ethanol. Oral administration of ethanol consistently induced damage in the rat glandular stomach and intestine. Zinc did not demonstrate effect per se and significantly reduced gastrointestinal lesions when administered either before or after lesion induction. Ethanol induced enhancement of thiobarbituric acid reactive substance and reactive species levels, diminished the ascorbic acid and total protein SH content as well as superoxide dismutase and catalase activity in stomach and intestine of rats. Zinc treatment prevented and reversed these alterations induced by ethanol. Stomach and intestine of rats treated with zinc presented higher zinc content than the tissues of rats treated only with ethanol. Non-protein SH content was not altered by any treatment. Results suggested that the gastrointestinal protective effect of zinc in this experimental model could be due to its antioxidant effect.

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Section: Discussionmentioning

confidence: 63%

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Ineu

Oliveira

et al. 2013

Food and Chemical Toxicology

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“…Enhanced apoptotic death of gastric epithelial cells has been partly implicated in ethanol-induced gastric mucosal injury [ 2 , 51 , 52 ]. Inflammatory signals along with oxidative stress have been reported to instigate the expression of several genes responsible for cellular death by apoptosis [ 4 , 53 ]. Apoptotic cascade is initiated by pro-apoptotic signals such as Bax [ 2 , 29 ] which favor the release of Cyt C from the mitochondria to the cytosol, with subsequent activation of caspase-9 and ultimately caspase-3, the major executioner caspase [ 3 , 14 ].…”

Section: Discussionmentioning

confidence: 99%

Diosmin Protects against Ethanol-Induced Gastric Injury in Rats: Novel Anti-Ulcer Actions

et al. 2015

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Alcohol consumption has been commonly associated with gastric mucosal lesions including gastric ulcer. Diosmin (DIO) is a natural citrus flavone with remarkable antioxidant and anti-inflammatory features that underlay its protection against cardiac, hepatic and renal injuries. However, its impact on gastric ulcer has not yet been elucidated. Thus, the current study aimed to investigate the potential protective effects of DIO against ethanol-induced gastric injury in rats. Pretreatment with DIO (100 mg/kg p.o.) attenuated the severity of ethanol gastric mucosal damage as evidenced by lowering of ulcer index (UI) scores, area of gastric lesions, histopathologic aberrations and leukocyte invasion. These actions were analogous to those exerted by the reference antiulcer sucralfate. DIO suppressed gastric inflammation by curbing of myeloperoxidase (MPO) and tumor necrosis factor-α (TNF-α) levels along with nuclear factor kappa B (NF-κB) p65 expression. It also augmented the anti-inflammatory interleukin-10 (IL-10) levels. Meanwhile, DIO halted gastric oxidative stress via inhibition of lipid peroxides with concomitant enhancement of glutathione (GSH), glutathione peroxidase (GPx) and the total antioxidant capacity (TAC). With respect to gastric mucosal apoptosis, DIO suppressed caspase-3 activity and cytochrome C (Cyt C) with enhancement of the anti-apoptotic B cell lymphoma-2 (Bcl-2) in favor of cell survival. These favorable actions were associated with upregulation of the gastric cytoprotective prostaglandin E2 (PGE2) and nitric oxide (NO). Together, these findings accentuate the gastroprotective actions of DIO in ethanol gastric injury which were mediated via concerted multi-pronged actions, including suppression of gastric inflammation, oxidative stress and apoptosis besides boosting of the antioxidant and the cytoprotective defenses.

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“…Suppression of the NF-κB pathway is considered a target for gastric ulcer treatment 43,44 immunoreactivity by PYR administration may show that it has gastroprotective effects by decreasing cytokine production.…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective Effects of Pear (Pyrus Communis L.) Extract on Ethanol Induced Gastric Ulcer in Rats

Eraslan¹

2021

jamp

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Various natural molecules have been examined against ethanol-induced gastric ulcer up to present. Pear, Pyrus communis L. (PYR), includes various antioxidant and anti-inflammatory features. Current study was planned to find out potential preventive properties of PYR extract against gastric ulcer induced by ethanol in rats. 32 rats were assigned to 4 groups (n=8). Group I was sham, group II was ulcer group. Groups III and IV were 4 and 8 ml/kg PYR groups. Group I, normal saline was administered and group II, III and IV were administered ethanol (5 ml/kg) by oral gavage to rats. Phenolic substances in PYR content were detected via high-pressure liquid chromatography (HPLC). CUPRAC, ABTS and FCR amounts of PYR extract were determined. Gastric tissue was evaluated through macroscopic and immunohistochemical methods. NF-kB and caspase-3 expressions increased in ulcer group but PYR treatment reversed these levels. PYR extract performed protective effects against ethanol-induced gastric ulcer by decreasing NF-kB and caspase-3 expressions and preventing gastric mucosal injury. As a result, PYR extract has been shown to have a strong therapeutic effect against gastric ulcer. Therefore, we propose PYR as a potential antiulcer drug.

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Protective effect of a cysteine prodrug and antioxidant, L-2-oxothiazolidine-4-carboxylate, against ethanol-induced gastric lesions in rats

Cited by 18 publications

References 52 publications

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Diosmin Protects against Ethanol-Induced Gastric Injury in Rats: Novel Anti-Ulcer Actions

Gastroprotective Effects of Pear (Pyrus Communis L.) Extract on Ethanol Induced Gastric Ulcer in Rats

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