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The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
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The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

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Effects of DHEA and DHEAS in Neonatal Hypoxic-Ischemic Brain Injury

Elena Mayer1, Ira Winkler1, Eva Huber1

  • 1Department of Pediatrics II (Neonatology), Medical University of Innsbruck, Anichstraße 35, 6020 Innsbruck, Austria.

Antioxidants (Basel, Switzerland)
|January 8, 2025
PubMed

Insights

Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) showed no significant neuroprotective effects in a neonatal brain injury model. However, these compounds demonstrated a safe profile, paving the way for further research.

Area of Science:

  • Neuroscience
  • Neonatal Medicine
  • Pharmacology

Background:

  • Neonatal brain injury presents a critical clinical challenge with limited therapeutic interventions.
  • Neurosteroids like dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) show promise based on adult models.
  • Understanding neurosteroid roles in neonatal injury is crucial for developing new treatments.

Purpose of the Study:

  • To evaluate the neuroprotective and antioxidant potential of DHEA and DHEAS.
  • To assess DHEA and DHEAS in a mouse model of neonatal hypoxic-ischemic brain injury.
  • To determine the safety and efficacy of DHEA and DHEAS in neonatal brain injury.

Main Methods:

  • Neonatal hypoxic-ischemic brain injury induced using the modified Rice-Vannucci model in 7-day-old mice.
  • Treatment with DHEA and DHEAS at doses of 0.1, 1, and 10 µg/g body weight via intraperitoneal injection.
  • Analysis included brain injury assessment, apoptosis, microglial activation, and oxidative/antioxidant markers (NOX2, 4-HNE, 8-OHdG, SOD1).

Main Results:

  • No statistically significant neuroprotective or antioxidant effects were observed for DHEA or DHEAS at the tested doses and time points.
  • DHEA and DHEAS exhibited no toxic or adverse effects in the neonatal mouse model.
  • The study established a safety profile for DHEA and DHEAS in this context.

Conclusions:

  • Current DHEA and DHEAS dosing and timing strategies were not effective in neonatal brain injury.
  • Further research is needed to optimize DHEA(S) delivery, dosage, and timing for potential neuroprotection.
  • Investigating the precise mechanisms of action and clinical applicability of DHEA(S) in neonatal care is warranted.

Keywords:
dehydroepiandrosteronedehydroepiandrosterone sulfatehypoxia–ischemiamouse modelneonatal hypoxic–ischemic brain injuryneuroprotection

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