Effect of Hypoxia in Uterus on the Expression of MBP and NF-H+L in the White Matter of Old Rats

Hypoxia in utero is a common problem in embryonic development. Early fetal and neonatal periods are periods of rapid brain growth and development, and their development depends on adequate oxygenation. The growth and development of the fetus in the mother’s uterus require an adequate supply of oxygen. Conversely, lack of oxygen can adversely affect fetal development. The purpose of this article is to study the effect of intrauterine hypoxia on the expression of MBP and NF-H+L in the white matter of the offspring of aged rats and establish a hypoxia model of SD rats through controlled experiments. Detect fetal rat blood gas and blood ion indexes and use immunohistochemistry to detect the expression of MBP and NF-H+L in the paraventricular white matter of the offspring of the offspring of rats. Parallel image analysis, and then observe the myelin sheath and axis in the offspring of the offspring under electron microscope ultrastructure of protrusions and microvessels. The results show that the main effect of intrauterine hypoxia can reduce the expression of MBP (1666.93, 2179.85, 432.72) and NF-H+L (721.266,1785.832, 246.512) in the offspring of the white matter in the elderly rats (all P<0.05)), MBP was highly positively correlated with NF-H+L (R=0.64, P<0.01). Observation by electron microscopy showed that compared with the blank control group, the offspring of the intrauterine hypoxia group showed more myelination, axon damage, and microvascular disease in the brain of the elder generation of rats. Therefore, intrauterine hypoxia can affect the expression of MBP and NF-H+L in the white matter of offspring in the offspring of the offspring, resulting in demyelination and damaged axons.

Prenatal Glucocorticoid Administration Accelerates the Maturation of Fetal Rat Hepatocyte

Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for maturation of 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 on the maturation of liver hepatocytes in preterm rats.Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real time-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, HNF4α, HGF, Thy-1, cyclin B, and CDK1 in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production.The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in premature fetuses.