944: Effect of antenatal progesterone on screening for Congenital Adrenal Hyperplasia (CAH) among preterm neonates

Abstract

+ saline (CTR, n¼8), saline + LPS (LPS, n¼9) and simvastatin + LPS (Simv + LPS, n¼7) groups. The simvastatin+saline group was not included because we do not anticipate the use of simvastatin alone. Six hours after the last injection, all mice were euthanized, pups quickly dissected and tissues collected. Fetal brains from each litter were pooled together. Tissues were homogenized and equal amounts of total protein were assayed using Luminex xMAP method for the phosphorylated p53, cJUN, JNK, STAT1, ATF2, p38, MEK1, HSP27, ERK, and MSK1. The median fluorescence intensity (MFI) was normalized to GAPDH control for each protein. One-Way or Kruskal-Wallis ANOVA with Holm-Sidak or Dunn's post-hoc tests as appropriate was used for analysis (statistical significance P<.05). RESULTS: Exposure to LPS lowered the protein expression of pATF2, pERK, pp53, pMEK1, pMSK, pSTAT1 and pc-Jun with pJNK reaching statistical significance (Figure). Simv rescued the levels of pATF2, pJNK and pc-Jun, but the results were not statistically significant. CONCLUSION: Prenatal exposure to LPS downregulates some proteins involved in MAPK signaling in fetal brain, indicating an effect on cellular proliferation, differentiation, survival, and death. Simvastatin partially prevented the LPS effect on these proteins. Further studies are needed to determine the mechanisms of the reported beneficial effects of statinsin the setting of preterm inflammation.