THE IMPACT OF VITAMIN D DEFICIENCY ON P65 NF-KB ACTIVITY IN THE PATHOGENESIS OF PLACENTAL DYSFUNCTION

Aim: To study the role of vitamin D in the activation of nuclear factor kB (NF-kB) as a factor in the development of placental disorders. Materials and methods: The study involved 135 women who were observed and gave birth at the Municipal Non-Profit Enterprise "Perinatal Center of Kyiv." The research was conducted as a case-control study, including 105 pregnant women in the main group with placental dysfunction (Group I – 70 women with vitamin D deficiency below 20 ng/ml, Group II – 35 women with vitamin D deficiency between 20 and 30 ng/ml) and 30 women in the control group with a physiological course of pregnancy and uncomplicated term deliveries. The concentration of 25(OH)D in the blood of pregnant women was measured using the immunoassay method with a Monobind reagent kit (USA) and a Sinnova ER 500 microplate reader (China). The determination of p65 NF-kB was carried out using the RayBio Human Procalcitonin ELISA method (RayBiotech, Inc., USA) with the Phospho-NF-kB P65 (Ser536) and Total NF-kB P65 ELISA Kit. Statistical analysis of the data was performed using the MedStat v.5.2 and EZR v.3.4.1 software. Initially, the normality of the data distribution was checked using the Shapiro-Wilk test, followed by the application of multiple comparisons using the Kruskal-Wallis rank-based one-way analysis of variance. Statistical significance was determined at p < 0.05. Results. The study revealed a significant difference in the levels of total and phosphorylated p65 NF-kB protein between the groups of pregnant women with vitamin D deficiency and the control group (p < 0.05). In pregnant women with vitamin D deficiency, there was a marked increase in the levels of total p65 NF-kB (median 69.5 pg/ml) and its activated form, indicating the activation of inflammatory processes in the placenta. Clinical manifestations of placental dysfunction, such as fetal growth restriction, preeclampsia, and preterm labor, were observed in one-third of the women with vitamin D deficiency. This was accompanied by changes in the hormonal function of the placenta (a decrease in progesterone and stabilization of placental lactogen) and morphological signs of placental abnormalities. The increase in p65 NF-kB activity was highest in women with placental abnormalities, particularly preeclampsia, fetal growth restriction, and preterm labor, indicating a link between vitamin D deficiency and inflammation in the placenta. Conclusion. Vitamin D levels below 20 ng/ml are associated with activation of the p65 NF-kB factor, which correlates with placental dysfunction, regardless of pregnancy outcomes. This confirms the role of vitamin D deficiency in the activation of NF-kB and the development of placental disorders.