Objective　To explore the protective effects of GYY4137, a new hydrogen sulfide donor, on intestinal mucosa in a neonatal rat model of necrotizing enterocolitis (NEC), and its potential mechanism. Methods　Sixty SD rats were randomly assigned into 4 groups: group A (control group), group B (NEC group), group C (NEC with GYY4137 treatment, H2S donor group), and group D (NEC with GYY4137 and Znpptreatment, HO-1 inhibitor group). The SD rat models of NEC were established using simulated milk feeding-hypoxia-cold stress-Lipopolysaccharides. The injury degree of intestinal mucosa was evaluated using HE-staining, and its mechanisms were investigated using biochemical indicators and Western blotting. Results　Compared with control group, the pathology score and the total superoxide dismutase (T-SOD) in the NEC group was significantly higher, the concentrations of methane dicarboxylic aldehyde (MDA) and necrosis factor α (TNF-α) were lower（P<0.05）. Compared with those in NEC group, the pathology score and the concentration of MDA and TNF-α in the H2S donor group were significantly lower, the T-SOD, and the HO-1 expression was higher. The pathology score and the level of MDA and TNF-α were significantly increased after treated with HO-1 inhibitor Znpp, and T-SOD was significantly decreased.. Conclusions　The GYY4137, as a new H2S donor, could attenuate the injury of intestinal mucosa in a neonatal rat model of NEC by upregulating the expression of HO-1.