Effects of antenatal glucocorticoids on the developing brain

被引：75

作者：

Carson, Ross ^{[1
]}

Monaghan-Nichols, A. Paula ^{[1
,2
]}

DeFranco, Donald B. ^{[1
,3
]}

Rudine, Anthony C. ^{[1
,4
]}

机构：

[1] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA

[2] Dept Neurobiol, Pittsburgh, PA USA

[3] Dept Pharmacol & Chem Biol, Pittsburgh, PA USA

[4] Dept Pediat, Div Newborn Med, Pittsburgh, PA USA

来源：

STEROIDS | 2016年 / 114卷

关键词：

Antenatal; Glucocorticoids; Preterm birth; Neurodevelopment; NEURAL STEM-CELLS; RESPIRATORY-DISTRESS-SYNDROME; OUTER SUBVENTRICULAR ZONE; GESTATIONAL-AGE; INDUCED HYPOMYELINATION; NEUROLOGIC DEFICITS; MULTIPLE COURSES; PROGENITOR CELLS; CORTICOSTEROIDS; OUTCOMES;

D O I：

10.1016/j.steroids.2016.05.012

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Glucocorticoids (GCs) regulate distinct physiological processes in the developing fetus, in particular accelerating organ maturation that enables the fetus to survive outside the womb. In preterm birth, the developing fetus does not receive sufficient exposure to endogenous GCs in utero for proper organ development predisposing the neonate to complications including intraventricular hemorrhage, respiratory distress syndrome (RDS) and necrotizing enterocolitis (NEC). Synthetic GCs (sGCs) have proven useful in the prevention of these complications since they are able to promote the rapid maturation of underdeveloped organs present in the fetus. While these drugs have proven to be clinically effective in the prevention of IVH, RDS and NEC, they may also trigger adverse developmental side effects. This review will examine the current clinical use of antenatal sGC therapy in preterm birth, their placental metabolism, and their effects on the developing brain. Published by Elsevier Inc.

引用

页码：25 / 32

页数：8

共 92 条

[71] Nongenomic glucocorticoid receptor action regulates gap junction intercellular communication and neural progenitor cell proliferation [J].