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Protective effects of hydrogen-rich saline on necrotizing enterocolitis in neonatal rats

机译:富氢盐水对新生大鼠坏死性小肠结肠炎的保护作用

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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.
机译:目的这项研究的目的是检验以下假设:富氢盐水(HRS)可能对新生大鼠模型中坏死性小肠结肠炎(NEC)的发展具有保护作用。方法配方喂养,暴露于窒息和冷应激的雄性新生Sprague-Dawley大鼠均可诱导NEC。六十四只幼崽随机分为四组:C + NS(n = 11),C + H2(n = 11),NEC + NS(n = 20)和NEC + H2(n = 22)。前两组分别由母鼠喂养。幼鼠接受腹膜内注射HRS(每天两次窒息前10分钟,每次10 ml / kg)或相同剂量的生理盐水。监测大鼠直至出生后96小时。评估体重,组织学NEC评分,存活时间,丙二醛,抗氧化能力,炎症介质和粘膜完整性。结果HRS治疗可保持体重,将NEC的发生率从85%(17/20)降低至54.5%(12/22),存活率从25%(5/20)增至68.2%(15/22) ,并减轻了NEC的严重性。此外,HRS抑制促炎介质(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,下调脂质过氧化,增强总抗氧化能力,并阻止二胺氧化酶增加。血清。但是,没有观察到HRS对白介素10 mRNA表达的显着影响。结论HRS通过减轻氧化应激,增加抗氧化能力,抑制炎症和保持黏膜完整性对NEC新生大鼠具有有益的作用。

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