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

AIM To explore the effect of hydrogen sulfide(H2S)on restraint water-immersion stress(RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate(ATP)-sensitive potassium(KATP)channels and nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB)pathway on such an effect.METHODS Male Wistar rats were randomly divided into a control group,a physiological saline(PS)group,a sodium hydrosulfide(Na HS)group,a glibenclamide(Gl)group,Gl plus Na HS group,a pyrrolidine dithiocarbamate(PDTC)group,and a PDTC plus Na HS group.Gastric mucosal injury was induced by RWIS for 3 h in rats,and gastric mucosal damage was analyzed after that.The PS,Na HS(100μmol/kg body weight),Gl(100μmol/kg body weight),Gl(100μmol/kg or 150μmol/kg body weight)plus Na HS(100μmol/kg body weight),PDTC(100μmol/kg body weight),and PDTC(100μmol/kg body weight)plus Na HS(100μmol/kg bodyweight)were respectively injected intravenously before RWIS.RESULTS RWIS induced serious gastric lesions in the rats in the PS pretreatment group.The pretreatment of Na HS(a H2S donor)significantly reduced the damage induced by RWIS.The gastric protective effect of the Na HS during RWIS was attenuated by PDTC,an NF-κB inhibitor,and also by glibenclamide,an ATP-sensitive potassium channel blocker,in a dose-dependent manner.CONCLUSION These results suggest that exogenous H2S plays a protective role against RWIS injury in rats,possibly through modulation of KATP channel opening and the NF-κB dependent pathway.