Protective effect of hydrogen sulfide against cold restraint stress-induced gastric mucosal injury in rats

Aboubakr, Esam M.; Taye, Ashraf; El‐Moselhy, Mohamed A.; Hassan, Magdy K.

doi:10.1007/s12272-013-0194-3

Cited by 17 publications

(12 citation statements)

References 38 publications

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“…In the dose range used in our present study NaHS exhibited vasodilatory properties as documented by dose-dependent increase in GBF that accompanied the protective activity of this compound suggesting that H 2 S is responsible for an increase in the GBF observed in our study. Our data are corroborative with recent report that NaHS administered intraperitoneally prevented cold restraint stress-induced oxidative gastric damage by the mechanism involving the inhibition of gastric acid and attenuation of reactive oxygen metabolites [ 31 ]. Lou et al .…”

Section: Discussionsupporting

confidence: 92%

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Endogenous Prostaglandins and Afferent Sensory Nerves in Gastroprotective Effect of Hydrogen Sulfide against Stress-Induced Gastric Lesions

et al. 2015

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Hydrogen sulfide (H2S) plays an important role in human physiology, exerting vasodilatory, neuromodulatory and anti-inflammatory effects. H2S has been implicated in the mechanism of gastrointestinal integrity but whether this gaseous mediator can affect hemorrhagic lesions induced by stress has been little elucidated. We studied the effect of the H2S precursor L-cysteine, H2S-donor NaHS, the H2S synthesizing enzyme (CSE) activity inhibitor- D,L-propargylglycine (PAG) and the gastric H2S production by CSE/CBS/3-MST activity in water immersion and restraint stress (WRS) ulcerogenesis and the accompanying changes in gastric blood flow (GBF). The role of endogenous prostaglandins (PGs) and sensory afferent nerves releasing calcitonin gene-related peptide (CGRP) in the mechanism of gastroprotection induced by H2S was examined in capsaicin-denervated rats and those pretreated with capsazepine to inhibit activity of vanilloid receptors (VR-1). Rats were pretreated with vehicle, NaHS, the donor of H2S and or L-cysteine, the H2S precursor, with or without the concurrent treatment with 1) nonselective (indomethacin) and selective cyclooxygenase (COX)-1 (SC-560) or COX-2 (rofecoxib) inhibitors. The expression of mRNA and protein for COX-1 and COX-2 were analyzed in gastric mucosa pretreated with NaHS with or without PAG. Both NaHS and L-cysteine dose-dependently attenuated severity of WRS-induced gastric lesions and significantly increased GBF. These effects were significantly reduced by pretreatment with PAG and capsaicin denervation. NaHS increased gastric H2S production via CSE/CBS but not 3-MST activity. Inhibition of COX-1 and COX-2 activity significantly diminished NaHS- and L-cysteine-induced protection and hyperemia. NaHS increased expression of COX-1, COX-2 mRNAs and proteins and raised CGRP mRNA expression. These effects of NaHS on COX-1 and COX-2 protein contents were reversed by PAG and capsaicin denervation. We conclude that H2S exerts gastroprotection against WRS-induced gastric lesions by the mechanism involving enhancement in gastric microcirculation mediated by endogenous PGs, sensory afferent nerves releasing CGRP and the activation of VR-1 receptors.

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Section: Discussionsupporting

confidence: 92%

“…Moreover, using similar experimental model of stress-induced gastric lesions, Aboubakr et al . [ 31 ] demonstrated that the inhibition of key enzyme of H 2 S synthesis, CSE with beta-cyano-L-alanine (BCA) exacerbated stress-induced gastric damage.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Prostaglandins and Afferent Sensory Nerves in Gastroprotective Effect of Hydrogen Sulfide against Stress-Induced Gastric Lesions

et al. 2015

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“…Apply it to the model of gastric mucosa damage to explore the potential mechanisms of H 2 S. By summarizing the experiments, we found that the conclusions between the different experiments are inconsistent. According to some research,26272829303132 NaHS played a protective effect in gastric mucosa damage. NaHS could decrease hemorrhagic damage, edema and epithelial cell loss induced by ethanol 26.…”

Section: Experimental Studies Of Hydrogen Sulfide In Gastric Mucosa Dmentioning

confidence: 99%

“…NaHS played a protective role through modulation of adenosine triphosphate-sensitive potassium channel opening and through the NF-κB dependent pathway 2728. It could reduce the serum level of TNF-α and interleukin-1β to abrogate the inflammatory 2930. It significantly decreased ulcer area31 and increased gastric blood flow at ulcer margin 3032.…”

Section: Experimental Studies Of Hydrogen Sulfide In Gastric Mucosa Dmentioning

confidence: 99%

The role of hydrogen sulfide in gastric mucosal damage

et al. 2019

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Gastrointestinal disease is a major global threat to public health. In the past few decades, numerous studies have focuses on the application of small molecule gases in the disease treatment. Increasing evidence has shown that hydrogen sulfide (H 2 S) has anti-inflammatory and anti-oxidative effects, and can regulate gastric mucosal blood flow in the gastric mucosa. After gastric mucosa damage, the level of H 2 S in the stomach decreases. Administration of H 2 S can protect and repair the damaged gastric mucosa. Therefore, H 2 S is a new target for the repair and treatment of gastric mucosa damage. In this review, we introduce the roles of H 2 S in the treatment of gastric mucosa damage and provide the potential strategies for further clinical treatment.

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“…NaHS (an H 2 S donor) attenuated ulcer index by reduction of gastric acid output, mucosal carbonyl content, pepsin activity and ROS generation. H 2 S also reduced tumoral necrosis factor (TNF)-alfa and myeloperoidase activity [ 41 ]. Recently, an attenuation of protective and hyperemic activity of NaHS in rats has been shown following capsaicin denervation.…”

Section: Introductionmentioning

confidence: 99%

Gut-Brain Axis in Gastric Mucosal Damage and Protection

Sgambato¹,

Capuano²,

Sullo³

et al. 2016

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BackgroundThe gut-brain axis plays a potential role in numerous physiological and pathological conditions. Several substances link stomach with central nervous system. In particular, hypothalamo-pituitary-adrenocortical axis, thyrotropin-releasing factor-containing nerve fibers and capsaicin-sensitive nerves are principal mediators of the harmful and protective central nervous system-mediated effects on gastric mucosa. Also, existing evidence indicates that nitric oxide, prostaglandins and calcitonin gene-related peptide play a role as final effectors of gastric protection.MethodsWe undertook a structured search of bibliographic databases for peer-reviewed research literature with the aim of focusing on the role of gut-brain axis in gastric damage and protection. In particular, we examined manuscripts dealing with the role of steroids, thyrotropin-releasing hormone, prostaglandins, melatonin, hydrogen sulfide and peptides influencing food intake (i.e. leptin, cholecystokinin, peptide YY, central glucagon–like peptide-1, and ghrelin). Also, the role of GABAergic and glutamatergic pathways in gastric mucosal protection have been examined.ResultsWe found and reviewed 61 peer-reviewed papers dealing with the major aspects related to the role of gut brain axis in gastric mucosal damage and protection.ConclusionsA dense neuronal network links stomach with central nervous system and a number of neurotransmitters and peptides functionally and anatomically related to central nervous system play a major role in contributing to gastric mucosal integrity.Exploiting the mechanisms underlying the connection between brain and gut may lead to a better understanding of the pathophysiology of gastric mucosal injury and to an improvement in the prevention and, eventually, management of gastric damage.

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Protective effect of hydrogen sulfide against cold restraint stress-induced gastric mucosal injury in rats

Cited by 17 publications

References 38 publications

Endogenous Prostaglandins and Afferent Sensory Nerves in Gastroprotective Effect of Hydrogen Sulfide against Stress-Induced Gastric Lesions

Endogenous Prostaglandins and Afferent Sensory Nerves in Gastroprotective Effect of Hydrogen Sulfide against Stress-Induced Gastric Lesions

The role of hydrogen sulfide in gastric mucosal damage

Gut-Brain Axis in Gastric Mucosal Damage and Protection

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