The impact of hydrogen sulfide in oesophagoprotection (840.15)

Abstract

Various studies have shown that novel cytoprotective gasotransmitter hydrogen sulfide (H2S) has cytoprotective and preventive effects in the gastrointestinal system (Wallace J., 2010‐2012). However, the mechanism of H2S on oesophageal barrier remains unclear. Therefore, the aim of present study was to examine the protective role of endogenous H2S in oeosphageal mucosal (OM) lesions related to stress‐associated injury and postprandial hyperglycemia (PHG) which we recently recognized as a serious trigger in the oesophageal injury genesis (Hrytcevych N., 2011‐2013). Aim: To determine whether or not H2S attenuates oesophageal mucosal cytoprotection in rats with nonerosive oeosphagitis and long term PHG, and explored the underlying mechanisms may be involved. Methods: Rats without and with 3,5 h water immersion and restraint stress (WIRS) and 28 days of PHG received i.p. of vehicle, cystathionine gama‐lyase (CSE) inhibitor, DL‐propargylglycine (PAG, 25 mg/kg i.p.), CBS inhibitor, beta‐cyano‐alanine (BCA, 50 mg/kg i.p.), or H2S donor NaHS (100 mlmol/kg) prior to WIRS. Scoring lesion index (LI), vascular index (VI) by OM histomorphology, IL‐10, IL‐17 by ELISA. Results: WIRS & PHG induced non‐erosive injury which characterized by rise LI and VI vs control. PAG or BCA pretreatment enhanced EM lesions escalating LI and VI in twice, drop IL‐10 and rise IL‐17. NaHS mediated decrease of OM lesions via decreased LI, VI and increase IL‐10 and decrease IL‐17 scores vs control. Conclusion: These results indicate that endogenous H2S plays oesophagoprotective role by inhibiting inflammation, oedeme and vasodilator effect, highlighting the therapeutic potential for H2S donor in postprandial hyperglycemic stress‐associated conditions.