Glucocorticoid exposure induces preeclampsia via dampening 1,25-dihydroxyvitamin D3.

The pathogenesis of preeclampsia (PE) involves a number of biological processes that may be directly or indirectly affected by glucocorticoid (GC) and vitamin D. GC exposure increases the risk of PE, and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) deficiency may result in PE. The purpose of the present study was to confirm the involvement of GC/1,25-(OH)2D3 axis in the pathogenesis of PE. In the study, cortisol levels of PE patients were found to be higher than that of non-complicated pregnancies, while 1,25-(OH)2D3 were decreased in both PE women and GC-induced PE rats. Mechanically, GC reduced 1,25-(OH)2D3 levels via disturbing its biosynthetic and catabolic enzymes, including Cyp3a1,Cyp24a1 and Cyp27b1, especially enhancing the expressions of Cyp3a1, the dominant enzyme for vitamin D degeneration. Moreover, replenishing 1,25-(OH)2D3 ameliorated the symptoms and placental oxidative stress of GC-induced rat PE. The protective actions of 1,25-(OH)2D3 might be explained by its roles in antagonizing the effects of GC on trophoblast proliferation and apoptosis. Together, these findings suggest that GC exposure could lead to PE via dampening 1,25-(OH)2D3 biosynthesis, and GC/1,25-(OH)2D3 axis might represent a common pathway through which PE occurs.

Expression of lung surfactant proteins SP-B and SP-C and their modulating factors in fetal lung of FGR rats.

This study investigated the expression of lung surfactant proteins SP-B and SP-C, and their modulating factors TTF-1 and PLAGL2 in the fetal lung of rats with fetal growth restriction (FGR). The rat FGR model was established by prenatal hypoxia in the first stage of pregnancy, 180 rats for experiment served as hypoxia group, and 197 healthy rats served as normal control group. The FGR incidence in hypoxia was compared with that in normal control group. The histological changes in the fetal lung were observed under the light microscope and electronic microscope in two groups. The SP-B, SP-C, TTF-1 and PLAGL2 proteins were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and mRNA in the fetal lung of two groups were detected by using Western blotting and RT-PCR respectively. The FGR rat model was successfully established by using hypoxia. Pathologically the fetal lung developed slowly, and the expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and mRNA in the fetal lung were significantly reduced in hypoxia group as compared with those in normal control group. It was suggested that maternal hypoxia in the first stage of pregnancy could induce FGR, and reduce the expression of SP-B and SP-C, resulting in the disorder of fetal lung development and maturation.