Okur H, Küçükaydin M, Köse K, Kontaş O, Doğam P, Kazez A
Department of Pediatric Surgery, Erciyes University Faculty of Medicine, Kayseri, Turkey.
J Pediatr Surg. 1995 Oct;30(10):1416-9. doi: 10.1016/0022-3468(95)90395-x.
The authors developed an experimental model of necrotizing enterocolitis (NEC) by hypoxia-reoxygenation, and determined the content of malondialdehyde levels as an index of lipid peroxidation, related with a free-radical reaction in the gastrointestinal tract of newborn rats. They also investigated the role of vitamin E, an antioxidant, in this free-radical injury. The study was performed on 1-day-old rats. The 30 rat pups were divided into three groups. Hypoxia was induced by placing the pups in a 100% carbon dioxide chamber for 5 minutes. The pups were reoxygenated with 100% oxygen for 5 minutes. Group 1 (n = 10) was subjected to hypoxia-reoxygenation and killed 3 days after hypoxia. Group 2 (n = 10) was subjected to hypoxia-reoxygenation and treated with vitamin E (30 IU/kg/d intraperitoneally) for the next 3 days, and killed. Group 3 (n = 10) rats served as controls. The histopathology of the intestinal lesions in group 1 animals was characteristic of ischemic injury and ranged from superficial epithelial damage with villous shortening to transmural necrosis. In the vitamin E-treated animals these lesions were milder. The malondialdehyde levels of group 1 were significantly higher than those of the other two groups (P < .001). This study shows that oxidant-mediated lipid peroxidation injury plays a central role in mediating hypoxia-induced intestinal necrosis and suggests that vitamin E may play a therapeutic role in NEC.
作者通过缺氧复氧建立了坏死性小肠结肠炎（NEC）的实验模型，并测定了丙二醛水平，作为脂质过氧化的指标，其与新生大鼠胃肠道中的自由基反应有关。他们还研究了抗氧化剂维生素E在这种自由基损伤中的作用。该研究在1日龄大鼠上进行。30只幼鼠被分为三组。通过将幼鼠置于100%二氧化碳 chamber 中5分钟来诱导缺氧。幼鼠用100%氧气复氧5分钟。第1组（n = 10）经历缺氧复氧，并在缺氧后3天处死。第2组（n = 10）经历缺氧复氧，并在接下来的3天内用维生素E（30 IU/kg/d腹腔注射）治疗，然后处死。第3组（n = 10）大鼠作为对照。第1组动物肠道病变的组织病理学表现为缺血性损伤特征，范围从伴有绒毛缩短的浅表上皮损伤到透壁坏死。在维生素E治疗的动物中，这些病变较轻。第1组的丙二醛水平显著高于其他两组（P <.001）。这项研究表明，氧化介导的脂质过氧化损伤在介导缺氧诱导的肠道坏死中起核心作用，并表明维生素E可能在NEC中发挥治疗作用。
