Abstract
Purpose
The aim of this study was to test the hypothesis that hydrogen-rich saline (HRS) might
have protective effects on the development of necrotizing enterocolitis (NEC) in a
neonatal rat model.
Methods
NEC was induced in male newborn Sprague–Dawley rats by formula feeding, exposure to
asphyxia and cold stress. Sixty-four rat pups were divided randomly into four groups:
C+NS (n=11), C+H2 (n=11), NEC+NS (n=20), and NEC+H2 (n=22). Rats in the former two groups were mother-fed. Pups received intra-peritoneal
injection of HRS (10 ml/kg, 10 min before asphyxia stress twice a day) or the same dose of normal saline. Rats were
monitored until 96 h after birth. Body weight, histological NEC score, survival time, malondialdehyde,
antioxidant capacity, inflammatory mediators, and mucosal integrity were assessed.
Results
HRS treatment maintained the body weight, reduced the incidence of NEC from 85% (17/20)
to 54.5% (12/22), increased the survival rate from 25% (5/20) to 68.2% (15/22), and
attenuated the severity of NEC. In addition, HRS inhibited the mRNA expression of
pro-inflammatory mediators (inducible nitric oxide synthase, tumor necrosis factor-α,
and interleukin-6), down-regulated lipid peroxidation, enhanced total antioxidant
capacity, and prevented the increase of diamine oxidase in serum. However, no significant
influence of HRS on the interleukin-10 mRNA expression was observed.
Conclusions
HRS showed beneficial effects on neonatal rats with NEC via decreasing oxidative stress,
increasing antioxidant capacity, suppressing inflammation, and preserving mucosal
integrity.
Key words
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Article info
Publication history
Accepted:
November 15,
2012
Received in revised form:
October 2,
2012
Received:
July 31,
2012
Footnotes
☆Conflict of interest: The authors declare no conflict of interest.
☆☆Funding: This work was supported by grants from Shanghai Science and Technology Commission (124119a6500), Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition (11DZ2260500).
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.