To explore the role of ferritin in placenta, serum and umbilical cord blood of pregnant women and the changes of oxidative stress injury as well as cell apoptosis in placenta in the pathogenesis of preeclampsia (PE).

Material and methods:
Sixty pregnant women with severe PE were assigned to early-onset and late-onset PE group. Another 60 cases of normal late pregnant women with similar gestational weeks were divided into early-onset and late-onset control groups. Maternal serum and fetal umbilical cord blood ferritin content was determined by automatic biochemical immunoassay system; mRNA expression levels of ferritin and ferritin heavy chain (FTH) were detected by reverse transcription real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). Western blot was used to detect the relative expression level of ferritin and apoptosis; the contents of total superoxide dismutase (T-SOD) and malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were detected by colorimetry.

Serum uric acid (UA) and creatinine (Cr) levels were significantly higher in PE groups than the controls. The serum ferritin levels were significantly higher in the blood sample and umbilical cord blood sample than the controls. However, the mRNA and protein levels of ferritin were significantly lower in placenta samples than the controls. The placental cleaved caspase-3 and Bcl-2 levels were significantly lower than those in the early onset PE group. The levels of GSH-Px and MDA in placenta were significantly higher. Finally, the neonatal outcomes of PE groups were worse than those in the early onset PE group.

Levels of ferritin in blood sample, umbilical cord blood and placenta tissues of PE patients were significantly different than levels in normal pregnant women. Factors related to oxidative stress and cell apoptosis in placenta tissues were also significantly different in PE cases. These results may assist understanding the pathogenesis of PE and provide potential biomarkers for diagnosis of PE.