Neonatal Intensive Care Unit, Zekai Tahir Burak Maternity Teaching Hospital, 06110 Hamamönü, Ankara, Turkey.
J Pediatr Surg. 2012 Sep;47(9):1652-7. doi: 10.1016/j.jpedsurg.2012.02.016.
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.
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.
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).
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.
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。
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。
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）。
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。
