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

        Esam M. Aboubakr,Ashraf Taye,Mohamed A. El-Moselhy,Magdy K. Hassan 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.12

        Hydrogen sulfide (H2S) is an endogenous gaseousmediator plays a potential role in modulating gastricinflammatory responses. However, its putative protectiverole remains to be defined. The present study aimed toevaluate role of the exogenously released and endogenouslysynthesized H2S in cold restraint stress (CRS)-induced oxidativegastric damage in rats. Rats were restrained, andmaintained at 4 C for 3 h. The H2S donor, sodium hydrosulfide(NaHS) (60 lmol/kg) was injected intraperitoneally(i.p.) before CRS. Our results revealed that NaHS pretreatmentsignificantly attenuated ulcer index, free and total acidoutput, and pepsin activity in gastric juice along withdecreased gastric mucosal carbonyl content and reactiveoxygen species production. This was accompanied byincreased gastric juice pH and mucin concentration inaddition to restoring the deficits in the gastric reduced glutathione,catalase as well as superoxide dismutase enzymeactivities. NaHS pretreatment markedly reduced the serumlevel of tumor necrosis factor (TNF-a) and myeloperoxidaseactivity compared to CRS-non-treated. Moreover, NaHSpreadministration significantly abrogated the inflammatoryand the deleterious responses of gastric mucosa in CRS. Theprotective effects of H2S were confirmed by gastric histopathologicalexamination. However, pretreatment withthe H2S-synthesizing enzyme, cystathionine-gamma-lyaseinhibitor, beta-cyano-L-alanine (50 mg/kg, i.p.) reversed thegastroprotection afforded by the endogenous H2S. Collectively, our results suggest that H2S can protect ratgastric mucosa against CRS-induced gastric ulcerationpossibly through mechanisms that involve anti-oxidant andanti-inflammatory actions alongside enhancement of gastricmucosal barrier and reduction in acid secretory parameters.

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