Prenatal Glucocorticoid Administration Accelerates Maturation in the Hepatocytes of Fetal Rats

Abstract Prenatal glucocorticoid (GC) is clinically administered to pregnant women at risk of preterm birth for maturation of the cardiopulmonary function. Preterm and low birth weight infants often experience liver dysfunction after birth because the liver is immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration regarding maturity of the liver in preterm rats. Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational day 17 and 19 before cesarean section. Real time polymerase chain reaction (RT-PCR) was then used to analyze the mRNA levels (albumin, HNF4α, HGF, Thy-1, cyclin B, and CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay (ELISA) were used to analyze protein production. Hepatocyte size enlarged because of growth and administration of prenatal DEX. Albumin, HNF4α, and hepatocyte growth factor (HGF) increased secondary to growth and administration of prenatal DEX. Cell cycle markers, cyclin B, and CDK1 gradually decreased during growth and by administration of DEX. These results suggest that prenatal GC administration achieves hepatocyte maturation via expression of HNF4α and HGF in premature fetuses.