期刊
SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep10871
关键词
-
资金
- National Natural Science Foundation of China [81471467, 30901617, 81473016, 81471504, 81172711]
- Anhui Medical University
- Grants for Scientific Research of BSKY [XJ201404]
It is increasingly recognized that vitamin D3 (VitD3) has an anti-inflammatory activity. The present study investigated the effects of maternal VitD3 supplementation during pregnancy on LPS-induced placental inflammation and fetal intrauterine growth restriction (IUGR). All pregnant mice except controls were intraperitoneally injected with LPS (100 mu g/kg) daily from gestational day (GD) 15-17. In VitD3 + LPS group, pregnant mice were orally administered with VitD3 (25 mu g/kg) before LPS injection. As expected, maternal LPS exposure caused placental inflammation and fetal IUGR. Interestingly, pretreatment with VitD3 repressed placental inflammation and protected against LPS-induced fetal IUGR. Further analysis showed that pretreatment with VitD3, which activated placental vitamin D receptor (VDR) signaling, specifically suppressed LPS-induced activation of nuclear factor kappa B (NF-kappa B) and significantly blocked nuclear translocation of NF-kappa B p65 subunit in trophoblast gaint cells of the labyrinth layer. Conversely, LPS, which activated placental NF-kappa B signaling, suppressed placental VDR activation and its target gene expression. Moreover, VitD3 reinforced physical interaction between placental VDR and NF-kappa B p65 subunit. The further study demonstrates that VitD3 inhibits placental NF-kappa B signaling in VDR-dependent manner. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity. Overall, the present study provides evidence for roles of VDR as a key regulator of placental inflammation.
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