, Volume 57, Issue 6, pp 1496-1503
Date: 22 Jan 2012

Gastroprotective Effect of NaHS Against Mucosal Lesions Induced by Ischemia–Reperfusion Injury in Rat

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Hydrogen sulfide (H2S) has been shown to display anti-inflammatory and antioxidant activities.


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.


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.


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.


Our findings indicate that a possible mechanism for the gastroprotective effect of H2S could be through the decreased mRNA expression and plasma release of proinflammatory cytokines.

Main finding: NaHS protects gastric mucosa on ischemia/reperfusion injury in rats by reducing the mRNA expression and plasma levels of pro-inflammatory cytokines.