Related Experiment Video
Updated: Feb 10, 2026
08:47
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
36.4K
Corticosteroids and perinatal hypoxic-ischemic brain injury
Katherine R Concepcion1, Lubo Zhang1
1Lawrence D. Longo, MD Center for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Drug Discovery Today
|May 21, 2018
Summary
Corticosteroids may offer new treatments for perinatal hypoxic-ischemic brain injury by modulating brain inflammation and apoptosis. This review explores their mechanisms and therapeutic potential for newborns.
Area of Science:
- Neuroscience
- Immunology
- Neonatal Medicine
Background:
- Perinatal hypoxic-ischemic (HI) brain injury is a leading cause of neonatal death and long-term neurological disability.
- Current therapeutic options for neonatal HI brain injury are limited.
- Neuroinflammation and apoptosis significantly contribute to HI brain injury pathophysiology.
Purpose of the Study:
- To review corticosteroid modulation of inflammation and apoptosis in the neonatal brain following HI.
- To explore the therapeutic potential of mineralocorticoid (MR) and glucocorticoid (GR) receptor targets.
Main Methods:
- Literature review of corticosteroid effects on neonatal brain inflammation and apoptosis.
- Analysis of immune cell involvement in HI brain injury.
- Identification of MR and GR targets for therapeutic strategies.
Main Results:
- Corticosteroids modulate key immune cells involved in the innate and adaptive immune response.
- MR and GR signaling pathways are critical in regulating neuroinflammation and apoptosis post-HI.
- Specific targets within MR and GR pathways show therapeutic promise.
Conclusions:
- Corticosteroids represent a promising therapeutic avenue for neonatal HI brain injury.
- Targeting MR and GR pathways could mitigate neuroinflammation and apoptosis.
- Further research into corticosteroid-mediated mechanisms may lead to effective infant treatments.
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