目的　观察新型外源性硫化氢（H2S）供体GYY4137对坏死性小肠结肠炎（NEC）大鼠肠黏膜的保护作用， 并探讨其可能的作用机制。方法　取60只健康新生SD大鼠，随机分成4组。正常对照组，不施加任何干预；NEC模型 组，通过人工喂养、缺氧、冷刺激、脂多糖方法制备NEC模型；H2S干预组，在NEC模型的基础上，腹腔注射H2S供体 GYY4137；血红素加氧酶-1 （HO-1）抑制剂组，在H2S干预组已有干预的基础上，腹腔注射HO-1抑制剂Znpp。于试验第 4天处死大鼠，取回盲部肠管进行苏木精-伊红（HE）染色并作组织病理学评分；检测各组新生鼠小肠组织中丙二醛（MDA） 及超氧化物歧化酶（SOD）含量，肿瘤坏死因子α（ TNF-α）水平以及肠道组织HO-1表达。结果　4组新生大鼠肠组织病 理评分的差异有统计学意义（P<0.001），NEC模型组的病理评分最高，其次为HO-1抑制剂组、 H2S干预组。NEC组病理 评分≥2，表明建模方法有效。NEC组与对照组相比，MDA及TNF-α含量明显上升，T-SOD含量下降，差异有统计学意义 （P<0.05）；H2S干预组同NEC组相比，MDA及TNF-α含量明显降低，T-SOD含量明显升高，HO-1表达增加，差异有统计 学意义（P<0.05）；HO-1抑制剂组较H2S干预组相比，MDA及TNF-α含量明显升高，T-SOD含量降低，差异有统计学意 义（P<0.05）。 结论　新型H2S供体GYY4137能够有效保护NEC大鼠肠黏膜，降低MDA及TNF-α的含量，增加T-SOD 的含量；其保护作用可能与上调HO-1蛋白的表达有关。

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.