Department of General Surgery, Children's Hospital of Shanghai, Shanghai Jiaotong University School of Medicine, Shanghai 200040, P. R. China.
J Pediatr Surg. 2013 Aug;48(8):1697-706. doi: 10.1016/j.jpedsurg.2012.11.038.
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.
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.
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.
HRS showed beneficial effects on neonatal rats with NEC via decreasing oxidative stress, increasing antioxidant capacity, suppressing inflammation, and preserving mucosal integrity.
本研究旨在验证富氢生理盐水(HRS)对新生大鼠坏死性小肠结肠炎(NEC)发展可能具有保护作用的假说。
通过配方喂养、窒息和冷应激使雄性新生 Sprague-Dawley 大鼠发生 NEC。64 只大鼠随机分为 4 组:C+NS(n=11)、C+H2(n=11)、NEC+NS(n=20)和 NEC+H2(n=22)。前两组大鼠采用母乳喂养。HRS (10 ml/kg,每日两次,每次窒息前 10 分钟腹腔注射)或等剂量生理盐水腹腔注射。监测大鼠至出生后 96 小时。评估体重、组织学 NEC 评分、生存时间、丙二醛、抗氧化能力、炎症介质和黏膜完整性。
HRS 治疗维持了体重,将 NEC 的发生率从 85%(17/20)降低至 54.5%(12/22),生存率从 25%(5/20)提高至 68.2%(15/22),并减轻了 NEC 的严重程度。此外,HRS 抑制了促炎介质(诱导型一氧化氮合酶、肿瘤坏死因子-α和白细胞介素-6)的 mRNA 表达,下调了脂质过氧化,增强了总抗氧化能力,并防止了血清中二胺氧化酶的增加。然而,HRS 对白细胞介素-10 mRNA 表达没有明显影响。
HRS 通过降低氧化应激、增加抗氧化能力、抑制炎症和维持黏膜完整性对患有 NEC 的新生大鼠具有有益作用。