Prenatal Lipopolysaccharide Increases Postnatal Intestinal Injury in a Rat Model of Necrotizing Enterocolitis
Prenatal Lipopolysaccharide Increases Postnatal Intestinal Injury in a Rat Model of Necrotizing Enterocolitis
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DOI：
10.1097/mpg.0b013e31818936b8
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发表时间：
2009-03-01
影响因子：
2.9
通讯作者：
Reber, Kristina M.
中科院分区：
文献类型：
--
作者：
Giannone, Peter J.;Nankervis, Tcraio A.;Reber, Kristina M.
背景：在患有绒毛膜氨基炎的母亲所生的婴儿中，坏死性小肠结肠炎 (NEC) 的发病率有所增加。假设：我们的目的是检验这样的假设：在 NEC 大鼠模型中，妊娠期间接触产前脂多糖的母亲所生的新生大鼠幼崽更容易受到肠道损伤，并且肠道损伤增加是由诱导型一氧化氮合酶失调介导的。方法：按时怀孕Sprague-Dawley 母鼠腹膜内注射 2 mg/kg 脂多糖或载体。每组母鼠的幼鼠均足月分娩并置于大鼠 NEC 模型中。一部分幼崽被给予载体或氨基胍。收获肠道并根据肠道损伤分级。结果：母体产前脂多糖暴露增加了新生大鼠NEC模型中肠道损伤的频率和严重程度。氨基胍治疗显着降低血浆一氧化氮水平。此外，氨基胍显着减少肠道损伤。结论：观察到的肠道损伤可能是通过一氧化氮合酶失调介导的。 JPGN 48：276-282，2009。
Background: An increased incidence of necrotizing enterocolitis (NEC) has been noted in infants who are born to mothers with chorioaminonitis.Hypothesis: Our objective was to test the hypothesis that newborn rat pups born to mothers exposed to prenatal lipopolysaccharide during pregnancy would be more susceptible to intestinal injury in a rat model of NEC and that the increased intestinal injury is mediated by dysregulation of inducible nitric oxide synthase.Methods: Time-dated pregnant Sprague-Dawley dams were given an intraperitoneal injection of either 2 mg/kg of lipopolysaccharide or vehicle. Rat pups from each group of dams were delivered at term and placed in a rat NEC model. A subset of pups was given either vehicle or aminoguanidine. Intestines were harvested and graded for decree of intestinal injury.Results: Maternal prenatal lipopolysaccharide exposure increased the frequency and severity of intestinal injury in the neonatal rat NEC model. Treatment with aminoguanidine significantly decreased plasma nitric oxide levels. Additionally, aminoguanidine significantly decreased intestinal injury.Conclusions: Intestinal injury observed may be mediated via nitric oxide synthase dysregulation. JPGN 48:276-282, 2009.