PMID- 24177262
OWN - NLM
STAT- MEDLINE
DCOM- 20140206
LR  - 20131209
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 224
IP  - 2
DP  - 2014 Jan 13
TI  - Folic acid supplementation during pregnancy protects against 
      lipopolysaccharide-induced neural tube defects in mice.
PG  - 201-8
LID - S0378-4274(13)01364-7 [pii]
LID - 10.1016/j.toxlet.2013.10.021 [doi]
AB  - Folic acid is a water-soluble B-complex vitamin. Increasing evidence demonstrates 
      that physiological supply of folic acid during pregnancy prevents folic acid 
      deficiency-related neural tube defects (NTDs). Previous studies showed that 
      maternal lipopolysaccharide (LPS) exposure caused NTDs in rodents. The aim of 
      this study was to investigate the effects of high-dose folic acid supplementation 
      during pregnancy on LPS-induced NTDs. Pregnant mice were intraperitoneally 
      injected with LPS (20 mug/kg/d) from gestational day (GD) 8 to GD12. As expected, 
      a five-day LPS injection resulted in 19.96% of fetuses with NTDs. Interestingly, 
      supplementation with folic acid (3mg/kg/d) during pregnancy significantly 
      alleviated LPS-induced NTDs. Additionally, folic acid significantly attenuated 
      LPS-induced fetal growth restriction and skeletal malformations. Additional 
      experiment showed that folic acid attenuated LPS-induced glutathione (GSH) 
      depletion in maternal liver and placentas. Moreover, folic acid significantly 
      attenuated LPS-induced expression of placental MyD88. Additionally, folic acid 
      inhibited LPS-induced c-Jun NH2-terminal kinase (JNK) phosphorylation and nuclear 
      factor kappa B (NF-kappaB) activation in placentas. Correspondingly, folic acid 
      significantly attenuated LPS-induced tumor necrosis factor (TNF)-alpha, interleukin 
      (IL)-1beta and IL-6 in placentas, maternal serum and amniotic fluid. In conclusion, 
      supplementation with high-dose folic acid during pregnancy protects against 
      LPS-induced NTDs through its anti-inflammatory and anti-oxidative effects.
CI  - Copyright (c) 2013 Elsevier Ireland Ltd. All rights reserved.
FAU - Zhao, Mei
AU  - Zhao M
AD  - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Anhui 
      Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, 
      China; School of Nursing, Anhui Medical University, Hefei 230032, China.
FAU - Chen, Yuan-Hua
AU  - Chen YH
FAU - Chen, Xue
AU  - Chen X
FAU - Dong, Xu-Ting
AU  - Dong XT
FAU - Zhou, Jun
AU  - Zhou J
FAU - Wang, Hua
AU  - Wang H
FAU - Wu, Shu-Xian
AU  - Wu SX
FAU - Zhang, Cheng
AU  - Zhang C
FAU - Xu, De-Xiang
AU  - Xu DX
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131028
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 935E97BOY8 (Folic Acid)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Cytokines/genetics
MH  - Dietary Supplements
MH  - Female
MH  - Fetal Growth Retardation/prevention & control
MH  - Folic Acid/*administration & dosage
MH  - Glutathione/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred ICR
MH  - NF-kappa B/metabolism
MH  - Neural Tube Defects/chemically induced/*prevention & control
MH  - Pregnancy
OTO - NOTNLM
OT  - Developmental toxicity
OT  - Folic acid
OT  - Inflammation
OT  - Lipopolysaccharide
OT  - Neural tube defects
OT  - Oxidative stress
EDAT- 2013/11/02 06:00
MHDA- 2014/02/07 06:00
CRDT- 2013/11/02 06:00
PHST- 2013/08/20 00:00 [received]
PHST- 2013/10/18 00:00 [revised]
PHST- 2013/10/21 00:00 [accepted]
PHST- 2013/11/02 06:00 [entrez]
PHST- 2013/11/02 06:00 [pubmed]
PHST- 2014/02/07 06:00 [medline]
AID - S0378-4274(13)01364-7 [pii]
AID - 10.1016/j.toxlet.2013.10.021 [doi]
PST - ppublish
SO  - Toxicol Lett. 2014 Jan 13;224(2):201-8. doi: 10.1016/j.toxlet.2013.10.021. Epub 
      2013 Oct 28.