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首页> 外文期刊>International Journal of Molecular Sciences >A Proposed Molecular Mechanism of High-Dose Vitamin D3 Supplementation in Prevention and Treatment of Preeclampsia
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A Proposed Molecular Mechanism of High-Dose Vitamin D3 Supplementation in Prevention and Treatment of Preeclampsia

机译：预防和治疗先兆子痫大剂量补充维生素D3的分子机制

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A randomized prospective clinical study performed on a group of 74 pregnant women (43 presenting with severe preeclampsia) proved that urinary levels of 15-F2t-isoprostane were significantly higher in preeclamptic patients relative to the control (3.05 vs. 2.00 ng/mg creatinine). Surprisingly enough, plasma levels of 25-hydroxyvitamin D3 in both study groups were below the clinical reference range with no significant difference between the groups. In vitro study performed on isolated placental mitochondria and placental cell line showed that suicidal self-oxidation of cytochrome P450scc may lead to structural disintegration of heme, potentially contributing to enhancement of oxidative stress phenomena in the course of preeclampsia. As placental cytochrome P450scc pleiotropic activity is implicated in the metabolism of free radical mediated arachidonic acid derivatives as well as multiple Vitamin D3 hydroxylations and progesterone synthesis, we propose that Vitamin D3 might act as a competitive inhibitor of placental cytochrome P450scc preventing the production of lipid peroxides or excess progesterone synthesis, both of which may contribute to the etiopathogenesis of preeclampsia. The proposed molecular mechanism is in accord with the preliminary clinical observations on the surprisingly high efficacy of high-dose Vitamin D3 supplementation in prevention and treatment of preeclampsia.
机译：对一组74名孕妇（43名患有严重先兆子痫的孕妇）进行的一项随机前瞻性临床研究表明，先兆子痫患者的尿中15-F 2t -异前列腺素的水平明显高于对照组（3.05对比2.00 ng / mg肌酐）。令人惊讶的是，两个研究组的血浆25-羟基维生素D 3 水平均低于临床参考范围，两组之间无显着差异。在离体胎盘线粒体和胎盘细胞系上进行的体外研究表明，细胞色素P450scc的自杀性自氧化可能导致血红素的结构分解，并可能在子痫前期过程中增强氧化应激现象。由于胎盘细胞色素P450scc的多效活性与自由基介导的花生四烯酸衍生物的代谢以及多种维生素D 3 羟基化和孕酮的合成有关，因此我们建议维生素D 3 可能作为胎盘细胞色素P450scc的竞争性抑制剂，防止脂质过氧化物的产生或孕酮的过量合成，这两者都可能导致先兆子痫的病因。该分子机制与大剂量维生素D 3 补充剂在预防和治疗先兆子痫中具有惊人疗效的初步临床观察相符。

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