Acute pancreatitis in pregnancy (APIP), which was thought to be rare, is becoming more frequent. In addition, high perinatal mortality among fetuses has been reported. Our research aimed to investigate and assess fetal lung injury in a rat model of APIP and its possible mechanisms. The APIP model was induced by sodium taurocholate in Sprague-Dawley rats during the third trimester. Sham-operated (SO) rats in late gestation were used as controls, and dynamic observation and detection in the SO and acute pancreatitis (AP) groups were performed at 3 time-points. Histological changes in the fetal lungs, as well as the maternal pancreas and placenta were assessed. The levels of serum amylase, lipase, TNF-α and IL-1β were detected in maternal rats, and the expression of surfactant proteins A, B, C and D as well as their mRNA were determined. In this study, fetal lung injury as well as maternal pancreas and placenta injuries occurred in a time-dependent manner. The levels of serum amylase, lipase and TNF-α were markedly increased in maternal rats, and the levels of surfactant proteins A, B, C and D in fetal lungs were significantly decreased in the fetal lungs of the AP group. Ultrastructure injuries and the dysregulated synthesis and secretion of pulmonary surfactant proteins were observed in the AP group. Our research suggests that fetal lung injury is involved in the rat model of APIP and that the dysregulated synthesis and secretion of pulmonary surfactant proteins play a critical role in fetal lung injury during APIP.
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