Abstract: Objective: To investigate the expression of IL-1β, IL-18 and TNF-α in maternal-fetal interface of preeclampsia (PE) pregnant women and the occurrence of mitophagy, and to explore the correlation between them. Methods: From June 2018 to February 2019, 35 normal pregnant women (control group), 33 mild PE pregnant women (mild PE group) and 37 severe PE pregnant women (severe PE group) hospitalized in Shenzhen Maternal and Child Health Hospital Affiliated to Southern Medical University were selected. The expression of IL-1β, IL-18 and TNF-α in serum was detected. The morphological changes of maternal-fetal interface inflammation were analyzed. The occurrence of mitophagy in placental trophoblasts was observed. RT-PCR and Western blotting were used to detect the expression of BNIP3, DRAM1 mRNA and their proteins, and the correlation between inflammatory mediators and mitophagy were analyzed. Results: The expression of IL-1β, IL-18 and TNF-α in serum of pregnant women in PE group was significantly higher than that of normal pregnant women (P＜ 0.01). The expression of IL-1β, IL-18 and TNF-α in severe PE group was significantly higher than that of mild PE group (P＜ 0.01). HE staining showed that the infiltration of inflammatory cells in placenta tissue of PE group was higher than that of control group; Transmission electron microscopy showed that the positive rate of mitophagy in severe PE group was (2.61±1.07)%, in mild PE group was (7.65±3.19)%, which were significantly lower than that in control group [(14.07±3.11)%，P＜0.01]. RT-PCR and Western blotting showed that the expression of BNIP3 and DRAM1 in PE pregnant women were down-regulated (P＜0.01). The correlation analysis showed a negative correlation between the expression of inflammatory mediators such as IL-1α, IL-18, TNF-α and the positive rate of mitophagy. Conclusions: The mitophagy activity of trophoblasts in PE pregnant women decreased, the accumulation of damaged mitochondria may lead to the increase of inflammatory mediators such as IL-1β, IL-18 and TNF-α at the maternal-fetal interface, which may be involved in the pathogenesis of PE.

Key words: Pre-eclampsia, Mitochondria;, Autophagy;, Inflammation;, Autophagosomes