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Related Experiment Video

Updated: Jan 13, 2026

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Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.

Teresa Hellberg1, Thomas Schmitz1, Christoph Bührer1

  • 1Department of Neonatology, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.

International Journal of Molecular Sciences
|January 10, 2026
PubMed
Summary

Cannabidiol (CBD) may protect preterm infants' hearts from oxygen-induced damage. Low-dose CBD (10 mg/kg) improved heart cell growth and structure, but higher doses were less effective. Sex differences influenced outcomes.

Keywords:
cannabidiol (CBD)cardiac remodelingcardiomyocyte proliferationneonatal hyperoxiaoxidative stress and inflammation

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Area of Science:

  • Neonatal physiology and cardiovascular development
  • Pharmacology and therapeutic interventions
  • Oxidative stress and inflammation research

Background:

  • Neonatal hyperoxia causes oxidative stress, inflammation, and disrupts cardiac maturation, leading to long-term cardiovascular issues in preterm infants.
  • Cannabidiol (CBD), a non-psychoactive compound, has shown organ protection in neonatal hyperoxia, but its cardiac effects are unknown.
  • Understanding CBD's impact on the developing heart is crucial for potential therapeutic applications in preterm neonates.

Purpose of the Study:

  • To investigate the cardioprotective effects of Cannabidiol (CBD) against hyperoxia-induced cardiac injury in a neonatal mouse model.
  • To determine if CBD can mitigate oxidative stress, inflammation, apoptosis, and adverse cardiac remodeling caused by neonatal hyperoxia.
  • To explore the dose-dependency and sex-specific effects of CBD in this neonatal injury model.

Main Methods:

  • Neonatal mice were exposed to 80% oxygen from postnatal day 5-7, receiving vehicle or CBD (10 or 30 mg/kg) or kept in room air.
  • Cardiac function, oxidative stress markers (Nrf2), inflammatory markers (IL1β, TNFα, IL6, CXCL1), apoptosis (Casp3, AIF), autophagy (Atg5, Atg12), and cardiomyocyte proliferation (Ki67) were assessed.
  • Histological analysis evaluated cardiac remodeling, including hypertrophy and fibrosis, at postnatal day 7 and 14.

Main Results:

  • Hyperoxia induced significant oxidative stress, inflammation, dysregulated apoptosis/autophagy, reduced cardiomyocyte proliferation, and adverse cardiac remodeling (hypertrophy, fibrosis).
  • CBD treatment attenuated hyperoxia-induced inflammation and normalized autophagy. The 10 mg/kg dose preserved cardiomyocyte proliferation and reduced heart wall thickness.
  • Both CBD doses reduced collagen deposition and apoptosis. Male mice showed more severe long-term impairments and responded better to low-dose CBD, indicating sex-specific effects.

Conclusions:

  • Cannabidiol (CBD) demonstrates potential cardioprotective effects against neonatal hyperoxia-induced cardiac injury.
  • A low dose of CBD (10 mg/kg) appears most effective, suggesting a narrow therapeutic window and highlighting dose-specific mechanisms.
  • Sex-dependent responses to CBD underscore the complexity of early cardiac maturation and the need for personalized therapeutic strategies.