Folic acid protects against lipopolysaccharide-induced preterm delivery and intrauterine growth restriction through its anti-inflammatory effect in mice.
Folic acid protects against lipopolysaccharide-induced preterm delivery and intrauterine growth restriction through its anti-inflammatory effect in mice.
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叶酸通过其抗炎作用防止小鼠脂多糖诱导的早产和宫内生长受限
DOI：
10.1371/journal.pone.0082713
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Xu DX
中科院分区：
文献类型：
--
作者：
Zhao M;Chen YH;Dong XT;Zhou J;Chen X;Wang H;Wu SX;Xia MZ;Zhang C;Xu DX
越来越多的证据表明，母亲在怀孕期间补充叶酸（FA）可以降低神经管缺陷的风险，但FA是否可以预防早产和宫内生长受限（IUGR）仍然不清楚。以往的研究表明，母体脂多糖（LPS）暴露可诱导啮齿类动物早产、胎儿死亡和IUGR。本研究的目的是探讨FA对LPS诱导的小鼠早产、死胎和IUGR的影响。部分孕鼠在注射LPS前1h经口给予FA（0.6、3或15 mg/kg）。如预期的，高剂量的LPS（300 μg/kg，i. p.）在妊娠第15天（GD 15），100%的母鼠在GD 18之前分娩，89.3%的胎仔死亡。低剂量LPS（75 μg/kg，i. p.）GD 15 ~ 17日每日1次，均出现IUGR。有趣的是，FA预处理可预防LPS诱导的早产和胎儿死亡。此外，FA显着减弱LPS诱导的IUGR。进一步的实验表明，FA抑制LPS诱导的小鼠胎盘核因子κ B（NF-κB）的活化。此外，FA抑制LPS诱导的人滋养层细胞系JEG-3中NF-κB活化。相应地，FA显着减弱LPS诱导的小鼠胎盘环氧化酶（考克斯）-2上调。此外，FA还显着降低了脂多糖处理小鼠羊水中白细胞介素（IL）-6和角质形成细胞源性细胞因子（KC）的水平。总的来说，孕妇在怀孕期间补充FA可以通过其抗炎作用防止LPS诱导的早产、胎儿死亡和IUGR。
Increasing evidence demonstrates that maternal folic acid (FA) supplementation during pregnancy reduces the risk of neural tube defects, but whether FA prevents preterm delivery and intrauterine growth restriction (IUGR) remains obscure. Previous studies showed that maternal lipopolysaccharide (LPS) exposure induces preterm delivery, fetal death and IUGR in rodent animals. The aim of this study was to investigate the effects of FA on LPS-induced preterm delivery, fetal death and IUGR in mice. Some pregnant mice were orally administered with FA (0.6, 3 or 15 mg/kg) 1 h before LPS injection. As expected, a high dose of LPS (300 μg/kg, i.p.) on gestational day 15 (GD15) caused 100% of dams to deliver before GD18 and 89.3% of fetuses dead. A low dose of LPS (75 μg/kg, i.p.) daily from GD15 to GD17 resulted in IUGR. Interestingly, pretreatment with FA prevented LPS-induced preterm delivery and fetal death. In addition, FA significantly attenuated LPS-induced IUGR. Further experiments showed that FA inhibited LPS-induced activation of nuclear factor kappa B (NF-κB) in mouse placentas. Moreover, FA suppressed LPS-induced NF-κB activation in human trophoblast cell line JEG-3. Correspondingly, FA significantly attenuated LPS-induced upregulation of cyclooxygenase (COX)-2 in mouse placentas. In addition, FA significantly reduced the levels of interleukin (IL)-6 and keratinocyte-derived cytokine (KC) in amniotic fluid of LPS-treated mice. Collectively, maternal FA supplementation during pregnancy protects against LPS-induced preterm delivery, fetal death and IUGR through its anti-inflammatory effects.
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影响因子：
7.3
作者：
Cella, M.;Farina, M. G.;Franchi, A. M.
通讯作者：
Franchi, A. M.
影响因子：
7.2
作者：
Nahum, Gerard G.;Uhl, Kathleen;Kennedy, Dianne L.
通讯作者：
Kennedy, Dianne L.
影响因子：
158.5
作者：
CZEIZEL, AE;DUDAS, I
通讯作者：
DUDAS, I
影响因子：
6
作者：
Carpentier, Pamela A.;Dingman, Andra L.;Palmer, Theo D.
通讯作者：
Palmer, Theo D.
影响因子：
9.8
作者：
Buhimschi, IA;Buhimschi, CS;Weiner, CP
通讯作者：
Weiner, CP