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Vitamin D restores angiogenic balance and decreases tumor necrosis factor‐α in a rat model of pre‐eclampsia
Author(s) -
Song Jing,
Li Yue,
An Ruifang
Publication year - 2017
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.13186
Subject(s) - medicine , endocrinology , oxidative stress , malondialdehyde , vascular endothelial growth factor , tumor necrosis factor alpha , inflammation , vitamin e , vitamin , eclampsia , vitamin d and neurology , proinflammatory cytokine , pregnancy , vegf receptors , antioxidant , biology , biochemistry , genetics
Aim Deficiency of vitamin D is correlated with pre‐eclampsia (PE), a hypertensive disorder of pregnancy, and is characterized by angiogenic imbalance and inflammation. The aim of this study was to investigate whether vitamin D supplementation can restore the angiogenic balance and ameliorate inflammation in a rat model of PE. Methods PE was induced using l ‐nitroarginine methylester. Normal pregnant and PE‐induced rats were supplemented with vitamin D on gestation days 14–19. Results Blood pressure was significantly increased in PE‐induced rats compared with normal pregnant rats ( P < 0.05), and vitamin D supplementation ameliorated this difference. In addition, rats from the PE group had lower vascular endothelial growth factor (VEGF; P < 0.01), and higher plasma‐soluble FMS‐like tyrosine kinase‐1 (sFlt‐1) and tumor necrosis factor‐α (TNF‐α; P < 0.01 for both) compared with the normal pregnant group. The vitamin D treatment group had significantly increased VEGF, and reduced sFlt‐1 and TNF‐α compared with the untreated PE group. Moreover, vitamin D supplementation was able to reduce the oxidative stress by lowering the plasma oxidative stress marker malondialdehyde. Conclusion Vitamin D supplementation plays an important role in restoring angiogenic balance and reducing inflammation in pregnancy‐induced hypertension.