Literature DB >> 22271414

Gastroprotective effect of NaHS against mucosal lesions induced by ischemia-reperfusion injury in rat.

Seyyed Ali Mard1, Niloofar Neisi, Ghasem Solgi, Maryam Hassanpour, Marjan Darbor, Maryam Maleki.   

Abstract

BACKGROUND: Hydrogen sulfide (H(2)S) has been shown to display anti-inflammatory and antioxidant activities. AIM: This study was designed to investigate the gastroprotective effect of sodium hydrosulfide (NaHS) on gastric mucosal lesions induced by ischemia-reperfusion (I/R) injury in rats and to determine the possible mechanism involved.
METHODS: Fifty-sex male Wistar rats were randomly assigned into sham, control (I/R injury), propargylglycine (PAG)-, L-cysteine-, and NaHS-treated groups. To induce I/R lesions, the celiac artery was first clamped for 30 min (ischemia phase), followed by removal of the clamp artery to allow reperfusion for 3 h. Treated rats received PAG [50 mg/kg, intravenous (i.v.)] or NaHS (160, 320, or 640 ng/kg, i.v.) 5 min before reperfusion. The effect of L-cysteine pretreatment was also investigated. Plasma levels of cytokines and cortisol were measured by an enzyme-linked immunosorbent assay. The gastric tissue samples were collected to quantify the mRNA expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor (TGF-β) by quantitative real-time PCR.
RESULTS: The total area of gastric lesions significantly decreased following the administration of NaHS and L-cysteine. The highest area of mucosal lesions was observed in PAG-treated rats. The mRNA expression and plasma levels of IL-1β and TNF-α were significantly decreased in L-cysteine- and NaHS-treated rats in a dose-dependent manner. Slightly increased levels of TGF-β were observed in these test groups, but the difference was not statistically significant compared with the other groups. The plasma level of cortisol was also not affected by NaHS treatment.
CONCLUSION: Our findings indicate that a possible mechanism for the gastroprotective effect of H(2)S could be through the decreased mRNA expression and plasma release of proinflammatory cytokines.

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Year:  2012        PMID: 22271414     DOI: 10.1007/s10620-012-2051-5

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  6 in total

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2.  Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function.

Authors:  John W Elrod; John W Calvert; Joanna Morrison; Jeannette E Doeller; David W Kraus; Ling Tao; Xiangying Jiao; Rosario Scalia; Levente Kiss; Csaba Szabo; Hideo Kimura; Chi-Wing Chow; David J Lefer
Journal:  Proc Natl Acad Sci U S A       Date:  2007-09-18       Impact factor: 11.205

3.  A protective role of hydrogen sulfide against oxidative stress in rat gastric mucosal epithelium.

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6.  Hydrogen sulfide enhances ulcer healing in rats.

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  6 in total
  31 in total

1.  Hydrogen sulfide: a rescue molecule for mucosal defence and repair.

Authors:  John L Wallace
Journal:  Dig Dis Sci       Date:  2012-06       Impact factor: 3.199

Review 2.  Modes of physiologic H2S signaling in the brain and peripheral tissues.

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3.  Gastric acid induces mucosal H2S release in rats by upregulating mRNA and protein expression of cystathionine gamma lyase.

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4.  Protective effects of exogenous NaHS against sepsis-induced myocardial mitochondrial injury by enhancing the PGC-1α/NRF2 pathway and mitochondrial biosynthesis in mice.

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6.  Hydrogen sulfide attenuates gastric mucosal injury induced by restraint water-immersion stress via activation of KATP channel and NF-κB dependent pathway.

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7.  Hydrogen sulphide protects against NSAID-enteropathy through modulation of bile and the microbiota.

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Review 8.  Hydrogen sulfide signaling in the gastrointestinal tract.

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Journal:  Antioxid Redox Signal       Date:  2013-05-19       Impact factor: 8.401

Review 9.  Chemical Biology of H2S Signaling through Persulfidation.

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10.  Toward More GI-Friendly Anti-Inflammatory Medications.

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