β-Naphthoflavone treatment attenuates neonatal hyperoxic lung injury in wild type and Cyp1a2-knockout mice.
β-Naphthoflavone treatment attenuates neonatal hyperoxic lung injury in wild type and Cyp1a2-knockout mice.
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DOI：
10.1016/j.taap.2017.11.017
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发表时间：
2018-01-15
影响因子：
3.8
通讯作者：
Couroucli XI
中科院分区：
文献类型：
--
作者：
Lingappan K;Maturu P;Liang YW;Jiang W;Wang L;Moorthy B;Couroucli XI
暴露于超生理浓度的氧气(高氧)会导致支气管肺发育不良(BPD)，这是早产儿最常见的肺部疾病之一，男性比女性更常见。β-萘黄酮(BNF)对成年和新生野生型(WT)小鼠以及Cyp1a1基因缺失的In和小鼠的高氧性肺损伤具有保护作用。在这项研究中，我们验证了脑神经营养因子治疗将减轻WT和CYP1A2−/−小鼠新生高氧性肺损伤的假设，并阐明了性别差异的影响。新生WT或CYP1A2−/−小鼠出生后第2~8天分别给予脑神经营养因子(10 mg/kg)或车用玉米油(CO)腹腔注射，隔日1次，同时在室内空气或高氧(85%O2)中维持14天。高氧暴露可导致WT和CYP1A2−/−小鼠肺泡简单，血管生成受阻，WT和CYP1A2−/−小鼠之间无明显差异。与类似暴露的雄性小鼠相比，−/−雌性小鼠在PND15有更好的肺血管生成保存。脑源性神经营养因子治疗减轻了两种基因型鼠的肺损伤和炎症，并且伴随着WT小鼠肝脏和肺组织细胞色素P1A1的显著诱导，但在细胞色素P1A2−/−小鼠中没有。与WT小鼠相比，碱性成纤维细胞生长因子处理提高了−/−小鼠肝脏中NADPH醌氧化还原酶(NQO1mRNA)的水平。这些结果表明，BNF对暴露于高氧环境中的新生小鼠具有保护作用，不依赖于CYP1A2，这可能与NQO1等II相酶的保护作用有关。
Exposure to supraphysiological concentrations of oxygen (hyperoxia) leads to bronchopulmonary dysplasia (BPD), one of the most common pulmonary morbidities in preterm neonates, which is more prevalent in males than females. Beta-naphthoflavone (BNF) is protective against hyperoxic lung injury in adult and neonatal wild type (WT) mice and in and mice lacking Cyp1a1gene. In this investigation, we tested the hypothesis that BNF treatment will attenuate neonatal hyperoxic lung injury in WT and Cyp1a2−/− mice, and elucidated the effect of sex-specific differences. Newborn WT or Cyp1a2−/− mice were treated with BNF (10 mg/kg) or the vehicle corn oil (CO) i.p., from postnatal day (PND) 2 to 8 once every other day, while being maintained in room air or hyperoxia (85% O2) for 14 days. Hyperoxia exposure lead to alveolar simplification and arrest in angiogenesis in WT as well as Cyp1a2−/− mice No significant differences were seen between WT and Cyp1a2−/− mice. Cyp1a2−/− female mice had better preservation of pulmonary angiogenesis at PND15 compared to similarly exposed males. BNF treatment attenuated lung injury and inflammation in both genotypes, and this was accompanied by a significant induction of hepatic and pulmonary CYP1A1 in WT but not in Cyp1a2−/− mice. BNF treatment increased NADPH quinone oxidoreductase (NQO1) mRNA levels in Cyp1a2−/− mouse livers compared to WT mice. These results suggest that BNF is protective in neonatal mice exposed to hyperoxia independent of CYP1A2 and this may entail the protective effect of phase II enzymes like NQO1.
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影响因子：
10
作者：
COONEY, TP;THURLBECK, WM
通讯作者：
THURLBECK, WM
DOI：
10.1165/ajrcmb.23.2.3904
发表时间：
2000-08-01
影响因子：
6.4
作者：
McGowan, S;Jackson, SK;Snyder, JM
通讯作者：
Snyder, JM
影响因子：
3.8
作者：
Maturu, Paramahamsa;Wei-Liang, Yanhong;Couroucli, Xanthi I.
通讯作者：
Couroucli, Xanthi I.
影响因子：
3.6
作者：
Jobe AH
通讯作者：
Jobe AH
影响因子：
4.5
作者：
Lingappan, Krithika;Jiang, Weiwu;Wang, Lihua;Couroucli, Xanthi I.;Moorthy, Bhagavatula
通讯作者：
Moorthy, Bhagavatula