Antenatal dexamethasone administration increases fetal lung DNA synthesis and RNA and protein content in nitrofen-induced congenital diaphragmatic hernia in rats

Antenatal glucocorticoids treatment has been shown to correct pulmonary imm aturity. The thymidine analog bromodeoxyuridine (BrdU) is incorporated into S-phase cells and used as a marker of DNA synthesis. In this study, we inv estigated the effect of antenatal glucocorticoid administration on DNA synt hesis and RNA and protein content in nitrofen-induced congenital diaphragma tic hernia (CDH) in rats to better understand the effect of antenatal gluco corticoids on CDH lung. The CDH model was induced in pregnant rats using ni trofen. Dexamethasone (0.25 mg/kg) was given on d 18.5 and 19.5 of gestatio n (term = 22 d). BrdU was administered 1 h before fetuses were killed on d 21, and detected by immunohistochemistry. DNA synthesis was evaluated by pe rcentage of BrdU-incorporated nuclei (BrdU labeling index). Total RNA and s oluble protein were extracted from another set of left lungs to measure RNA and protein content. BrdU labeling index and total RNA content were signif icantly decreased in CDH lung compared with control rats. Antenatal dexamet hasone treatment significantly increased BrdU labeling index and RNA and pr otein content in the left CDH lung. Our findings of decreased DNA synthesis and decreased RNA and protein content in CDH lung suggest that lung growth and development are suppressed in hypoplastic CDH lung. Increased DNA synt hesis and increased RNA and protein content in dexamethasone-treated CDH lu ng suggest that antenatal glucocorticoids may accelerate fetal lung growth and development in CDH.