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A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
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Brain injury caused by chronic fetal hypoxemia is mediated by inflammatory cascade activation

Rong Guo1, Weijian Hou, Yafeng Dong

  • 1Department of Pathophysiology, Xian Jiaotong University School of Medicine, Xian, Shannxi, PR China.

Reproductive Sciences (Thousand Oaks, Calif.)
|April 3, 2010
PubMed

Insights

Chronic fetal hypoxemia (CHX) triggers an inflammatory response in the fetal brain, leading to increased apoptosis and neuronal loss. This suggests CHX-induced brain injury results from an adaptive response that becomes harmful.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Perinatal Medicine

Background:

  • Cerebral palsy (CP) prevalence is linked to preterm birth, infection/inflammation, and fetal growth restriction (IUGR), a marker for chronic fetal hypoxemia (CHX).
  • CHX has been previously shown to induce a fetal inflammatory response syndrome (FIRS).

Purpose of the Study:

  • To investigate the hypothesis that chronic fetal hypoxemia (CHX) causes fetal brain injury via upregulation of inflammatory cytokine cascades and apoptosis.
  • To elucidate the mechanisms underlying CHX-induced fetal brain damage.

Main Methods:

  • Time-mated guinea pigs were exposed to normoxia (12% O2) or hypoxia (10.5% O2) during the final 21% of gestation.
  • Biochemical markers of oxidative stress (lactate/pyruvate and glutathione ratios) were assessed.
  • Hippocampal neuron density was quantified.
  • Gene expression of cytokines and receptors was analyzed using microarrays and confirmed with quantitative PCR (qPCR).

Main Results:

  • Chronic fetal hypoxemia induced a prooxidant state, evidenced by increased lactate/pyruvate and decreased glutathione ratios.
  • A significant decrease (>30%) in hippocampal neuron density was observed in hypoxemic fetuses.
  • CHX upregulated 22 inflammatory genes, with expression levels proportional to the degree of hypoxia.
  • Increased apoptosis and neuronal loss were characteristic of CHX-induced fetal brain inflammation.

Conclusions:

  • CHX initiates fetal brain inflammation, characterized by increased apoptosis and neuronal loss, which is inversely proportional to the severity of hypoxia.
  • Fetal brain injury associated with CHX may not be a direct result of oxygen deprivation but rather a maladaptive inflammatory response.
  • These findings offer insights into the pathogenesis of CP and potential therapeutic targets.

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