Hydrogen sulfide protects intestinal mucosa in a neonatal rat model of necrotizing enterocolitis by upregulating the expression of HO-1
10.3969/j.issn.1000-3606.2017.02.015
- VernacularTitle:H2S通过上调HO-1表达保护坏死性小肠结肠炎大鼠肠黏膜
- Author:
Zhaojun ZENG
;
Sen ZHONG
;
Jianing WANG
;
Junming TANG
;
Lei ZHANG
;
Jintang WANG
;
Yang ZHAO
- Keywords:
necrotizing enterocolitis;
hydrogen sulflde;
hemeoxygenase-1;
rat
- From:
Journal of Clinical Pediatrics
2017;35(2):138-142
- CountryChina
- Language:Chinese
-
Abstract:
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 signiflcantly lower, the T-SOD, and the HO-1 expression was higher. The pathology score and the level of MDA and TNF-α were signiflcantly increased after treated with HO-1 inhibitor Znpp, and T-SOD was signiflcantly 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.
