The protective effects of Ferrostatin-1 against inï¬ammation-induced preterm birth and fetal brain injury.
J Reprod Immunol
; 164: 104260, 2024 Aug.
Article
in En
| MEDLINE
| ID: mdl-38761507
ABSTRACT
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.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Phenylenediamines
/
Placenta
/
Brain Injuries
/
Lipopolysaccharides
/
Cyclohexylamines
/
Premature Birth
/
Ferroptosis
Limits:
Animals
/
Female
/
Humans
/
Pregnancy
Language:
En
Journal:
J Reprod Immunol
/
J. reprod. immunol
/
Journal of reproductive immunology
Year:
2024
Document type:
Article