PMID- 30738993 OWN - NLM STAT- MEDLINE DCOM- 20190705 LR - 20190705 IS - 1878-1705 (Electronic) IS - 1567-5769 (Linking) VI - 69 DP - 2019 Apr TI - Oral cholecalciferol supplementation alleviates lipopolysaccharide-induced preterm delivery partially through regulating placental steroid hormones and prostaglandins in mice. PG - 235-244 LID - S1567-5769(19)30051-7 [pii] LID - 10.1016/j.intimp.2019.01.052 [doi] AB - Several epidemiological reports demonstrated that vitamin D deficiency elevated risk of preterm delivery. We investigate the effects of oral cholecalciferol (VD3) supplementation on lipopolysaccharide (LPS)-induced preterm delivery. Pregnant mice were randomly assigned to either oral VD3 (25 mug/kg) or corn oil once daily from gestational day (GD)13 to GD15, and were intraperitoneally injected with either LPS (200 mug/kg) or normal saline on GD15. As expected, LPS was effective in inducing preterm delivery and fetal death. LPS-induced preterm delivery and fetal death were alleviated in VD3-pretreated mice. LPS-induced down-regulation of genes for placental progesterone biosynthetic enzymes was blocked in VD3-pretreated mice. LPS-induced reduction of serum progesterone was correspondingly attenuated by VD3. Although oral VD3 had no effect on estradiol production, it attenuated LPS-induced up-regulation of placental ERbeta in mice. LPS-induced placental COX-2 up-regulation and serum PGF2alpha elevation were alleviated in VD3-pretreated mice. Additionally, LPS-evoked elevations of the placental Tnfalpha, Il1beta, Mcp1 and Mip2 mRNAs were attenuated by VD3. VD3 promoted placental vitamin D receptor nuclear translocation and simultaneously alleviated LPS-induced nuclear translocation of NF-kappaB p65 and p50 subunits. These results provide evidence that oral VD3 supplementation alleviates LPS-induced preterm delivery and fetal demise partially through regulating placental steroid hormones and prostaglandins. CI - Copyright (c) 2019. Published by Elsevier B.V. FAU - Fu, Lin AU - Fu L AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology, Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, China. FAU - Chen, Yuan-Hua AU - Chen YH AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology, Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China; Department of Histology and Embryology, Anhui Medical University, Hefei 230032, China. Electronic address: yuanhuach@126.com. FAU - Xu, Shen AU - Xu S AD - Second Affiliated Hospital, Anhui Medical University, Hefei 230032, China. FAU - Yu, Zhen AU - Yu Z AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, China. FAU - Zhang, Zhi-Hui AU - Zhang ZH AD - Second Affiliated Hospital, Anhui Medical University, Hefei 230032, China. FAU - Zhang, Cheng AU - Zhang C AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology, Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, China. FAU - Wang, Hua AU - Wang H AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology, Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, China. FAU - Xu, De-Xiang AU - Xu DX AD - Department of Toxicology, Anhui Medical University, Hefei 230032, China; Key Laboratory of Environmental Toxicology, Anhui Higher Education Institutes, Anhui Medical University, Hefei 230032, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Hefei 230032, China. Electronic address: xudex@126.com. LA - eng PT - Journal Article DEP - 20190207 PL - Netherlands TA - Int Immunopharmacol JT - International immunopharmacology JID - 100965259 RN - 0 (Lipopolysaccharides) RN - 0 (Prostaglandins) RN - 0 (Receptors, Calcitriol) RN - 1C6V77QF41 (Cholecalciferol) RN - 4G7DS2Q64Y (Progesterone) RN - 4TI98Z838E (Estradiol) SB - IM MH - Administration, Oral MH - Animals MH - Cholecalciferol/*therapeutic use MH - *Dietary Supplements MH - Estradiol/metabolism MH - Female MH - Humans MH - Inflammation MH - Lipopolysaccharides/immunology MH - Mice MH - Mice, Inbred ICR MH - Placenta/*metabolism MH - Pregnancy MH - Premature Birth/*diet therapy MH - Progesterone/metabolism MH - Prostaglandins/metabolism MH - Receptors, Calcitriol/*metabolism OTO - NOTNLM OT - Cholecalciferol OT - Inflammation OT - Lipopolysaccharide OT - Preterm delivery OT - Vitamin D receptor EDAT- 2019/02/11 06:00 MHDA- 2019/07/06 06:00 CRDT- 2019/02/11 06:00 PHST- 2019/01/08 00:00 [received] PHST- 2019/01/24 00:00 [revised] PHST- 2019/01/30 00:00 [accepted] PHST- 2019/02/11 06:00 [pubmed] PHST- 2019/07/06 06:00 [medline] PHST- 2019/02/11 06:00 [entrez] AID - S1567-5769(19)30051-7 [pii] AID - 10.1016/j.intimp.2019.01.052 [doi] PST - ppublish SO - Int Immunopharmacol. 2019 Apr;69:235-244. doi: 10.1016/j.intimp.2019.01.052. Epub 2019 Feb 7.