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N-乙酰半胱氨酸在坏死性小肠结肠炎新生大鼠模型中的抗氧化作用。

Antioxidant effects of N-acetylcysteine in a neonatal rat model of necrotizing enterocolitis.

机构信息

Neonatal Intensive Care Unit, Zekai Tahir Burak Maternity Teaching Hospital, 06110 Hamamönü, Ankara, Turkey.

出版信息

J Pediatr Surg. 2012 Sep;47(9):1652-7. doi: 10.1016/j.jpedsurg.2012.02.016.

Abstract

BACKGROUND/PURPOSE: Hypoxia and ischemia appear to play an important role in the pathogenesis of necrotizing enterocolitis (NEC), which may be related to oxygen-derived free radical formation. This study was designed to evaluate the role of oxidative stress and potentially beneficial effects of N-acetylcysteine (NAC) in a neonatal rat model of NEC.

METHODS

Thirty Wistar albino rat pups were randomly divided into 3 groups: group 1, control; group 2, NEC and saline; and group 3, NEC and NAC treatment. Necrotizing enterocolitis was induced by hyperosmolar enteral formula feeding and exposure to hypoxia after cold stress at 4°C and oxygen. The pups were killed on the fourth day, and their intestinal tissues were harvested for biochemical and histopathologic analysis.

RESULTS

Mucosal injury scores and intestinal malondialdehyde levels in group 2 were found to be significantly higher than that in other groups (P ≤ .05). Intestinal superoxide dismutase activities in group 3 were significantly higher than that in group 2 (P = .018). Intestinal tissue tumor necrosis factor α levels were significantly reduced with NAC treatment in group 3 compared with group 2 (P < .003).

CONCLUSIONS

It is likely that oxidative stress and inflammatory mediators contribute to the pathogenesis of NEC and that NAC has a protective effect on intestinal injury through its antiinflammatory and antioxidant properties.

摘要

背景/目的:缺氧和缺血似乎在坏死性小肠结肠炎 (NEC) 的发病机制中起重要作用,这可能与氧衍生自由基的形成有关。本研究旨在评估氧化应激在 NEC 新生大鼠模型中的作用以及 N-乙酰半胱氨酸 (NAC) 的潜在有益作用。

方法

将 30 只 Wistar 白化大鼠幼崽随机分为 3 组:第 1 组,对照组;第 2 组,NEC 和生理盐水;第 3 组,NEC 和 NAC 治疗组。通过高渗肠内配方喂养和在 4°C 和氧气下冷应激后,使幼崽发生 NEC。第 4 天处死幼崽,并采集其肠道组织进行生化和组织病理学分析。

结果

第 2 组的黏膜损伤评分和肠道丙二醛水平明显高于其他组(P≤0.05)。第 3 组的肠超氧化物歧化酶活性明显高于第 2 组(P=0.018)。与第 2 组相比,第 3 组的 NAC 治疗显著降低了肠道组织肿瘤坏死因子 α 水平(P<0.003)。

结论

氧化应激和炎症介质可能有助于 NEC 的发病机制,并且 NAC 通过其抗炎和抗氧化特性对肠道损伤具有保护作用。

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