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Updated: Jun 26, 2025
A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
Published on: November 19, 2019
The protective effects of Ferrostatin-1 against inflammation-induced preterm birth and fetal brain injury
Chaolu Chen1, Shuaiying Zhu1, Tiantian Fu1
1Department of Obstetrics and Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Zhejiang 310006, China.
Insights
Ferrostatin-1 (Fer-1) prevents preterm birth and fetal brain injury by inhibiting ferroptosis and maternal inflammation. This novel therapeutic strategy improves placental function and neurodevelopmental outcomes in offspring.
Area of Science:
- Reproductive biology
- Neuroscience
- Cellular biology
Background:
- Ferroptosis, a regulated cell death pathway, is implicated in preterm birth.
- The precise mechanisms linking ferroptosis to preterm birth and fetal brain injury are not fully understood.
- Ferrostatin-1 (Fer-1) is a known inhibitor of ferroptosis.
Purpose of the Study:
- To investigate the therapeutic potential of Fer-1 in mitigating preterm birth and associated fetal brain damage.
- To elucidate the role of placental ferroptosis in the pathogenesis of preterm birth.
- To assess the impact of Fer-1 on neurodevelopmental outcomes in offspring.
Main Methods:
- Analysis of human placental samples and clinical data to correlate ferroptosis with preterm birth.
- Utilizing a lipopolysaccharide (LPS)-induced preterm birth mouse model to evaluate Fer-1's protective effects.
- Examining fetal brain tissues and offspring neurodevelopmental function at 5 and 8 weeks post-birth.
Main Results:
- Placental ferroptosis was identified as a significant factor associated with preterm birth.
- Fer-1 administration effectively inhibited preterm birth by reducing placental ferroptosis and maternal inflammation.
- Antenatal Fer-1 treatment prevented acute fetal brain damage and improved long-term neurodevelopmental impairments.
Conclusions:
- Fer-1 demonstrates therapeutic efficacy in preventing preterm birth and fetal brain injury.
- Inhibition of maternal inflammation and enhancement of placental function are key mechanisms of Fer-1's action.
- Fer-1 represents a promising novel therapeutic strategy for managing preterm birth and its complications.
Introduction:
Recent studies have suggested the involvement of ferroptosis in preterm birth. Despite compelling evidence, the underlying mechanism remains unknown. This investigation aimed to determine the therapeutic effects of Ferrostatin-1 (Fer-1), an inhibitor of ferroptosis, in preterm birth and fetal brain injury.
Methods:
Human placenta samples and clinical data of participants were collected to ascertain whether placental ferroptosis was associated with preterm birth. Lipopolysaccharide (LPS)-induced preterm birth mouse model was used to examine the protective effects of Fer-1 on preterm birth. Fetal brain tissues and offspring mice at 5 and 8 weeks were studied to determine the effects of Fer-1 on the cognitive function of offspring.
Results:
We examined the mechanism of spontaneous preterm birth and discovered that placental ferroptosis was associated with preterm birth. Fer-1 inhibited preterm birth by ameliorating placental ferroptosis and maternal inflammation, thus improving LPS-induced intrauterine inflammation to maintain pregnancy. Antenatal administration of Fer-1 prevented LPS-induced fetal brain damage in the acute phase and improved long-term neurodevelopmental impairments by improving placental neuroendocrine signaling and maintaining placental function.
Conclusion:
Fer-1 inhibited preterm birth and fetal brain injury by inhibiting maternal inflammation and improving placental function. Our findings provide a novel therapeutic strategy for preterm birth.
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