Hydrogen Sulfide Protects The Intestinal Mucosa Of NEC Rats By Activation The Nrf2-ARE/HO-1 Pathway

Objective:To observe the protective effect of GYY4137,a new hydrogen sulfide donor（H₂S）,on the neonatal rats in a model of necrotizing enterocolitis（NEC）,and to study the potential mechanism.Methods:Seventy SD rats were randomly assigned into 5 groups（10 rats in the control group）: group A（control group）,group B（NEC group）,group C（NEC with GYY4137,H₂S donor group）,group D（NEC with GYY4137 and ATRA,Nrf2-ARE inhibitor group）,group E（NEC with GYY4137 and Znpp,HO-1 inhibitor group）.The rat model of NEC was established by using simulated milk feeding-hypoxia-cold stress-lipopolysaccharid.The injury degree of intestinal mucosa was evaluated by using HE-staining,and its mechanisms were investigated by using biochemistry indicators and western blotting.Results:Compared with those in control group,in the NEC group,the pathology score was increased,the levels of MDA,TNF-α and IL-6 were significantly higher,the vitality of T-SOD was decreased（P<0.05）.Compared with those in NEC group,in the H₂S donor group,the pathology score was significantly lower,the vitality of T-SOD was obviously increased,while the concentration of MDA,TNF-α and IL-6 were significantly decreased（P<0.05）,the expressions of Nrf2 and HO-1 were upregulated.The pathology score was increased after treated with ATRA or Znpp,the vitality of T-SOD was significantly decreased,and the levels of MDA,TNF-α and IL-6 were significantly increased（P<0.05）.There was no significant difference between the ATRA group and the Znpp group（P>0.05）.Conclusion:The GYY4137,as a new H₂S donor,attenuated the injury of intestinal mucosa in a neonatal rat model of NEC by activation the signal pathway Nrf2-ARE/HO-1.