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Published on: July 30, 2016
Prenatal Melatonin Therapy Enhances Postnatal Lung Development in a Mouse Model of Inflammation-Induced Preterm Birth
So Hee Park1, Hee Young Cho2, Jin Hyun Jun3
1Departments of Life Science, Graduate School, CHA University, Seongnam 13488, Republic of Korea.
Insights
Melatonin significantly reduces inflammation-induced preterm birth (IPTB) in mice. It also improves fetal lung development and surfactant production, offering potential benefits for neonatal pulmonary outcomes.
Area of Science:
- Reproductive Biology
- Neonatal Development
- Pulmonary Medicine
Background:
- Inflammation-induced preterm birth (IPTB) severely impacts neonatal lung development, leading to impaired pulmonary function.
- Current treatments for lung maturation in preterm infants lack efficacy and safety.
- Melatonin's anti-inflammatory and antioxidant properties suggest potential benefits, but its effects on fetal lung maturation are not well understood.
Purpose of the Study:
- To evaluate the therapeutic efficacy of melatonin in preventing IPTB and improving fetal lung maturation in a mouse model.
- To investigate melatonin's impact on inflammatory markers, placental function, and lung development in IPTB.
Main Methods:
- A mouse model of intrauterine inflammation-induced preterm birth (IPTB) using lipopolysaccharide (LPS) was established.
- Pregnant mice at gestational day 17 received LPS, with or without melatonin treatment.
- Uterine and fetal lung tissues were analyzed for molecular and histological changes at various time points.
Main Results:
- Melatonin significantly reduced the rate of preterm birth induced by LPS.
- Melatonin downregulated pro-inflammatory genes, restored placental blood flow, and increased lamellar body counts in fetal lungs.
- Melatonin treatment improved fetal lung structure, enhanced surfactant protein B expression, and promoted lung development in surviving offspring.
Conclusions:
- Melatonin effectively prevents inflammation-induced preterm birth in a mouse model.
- Melatonin mitigates uterine inflammation and supports fetal lung maturation, improving pulmonary outcomes.
- Melatonin demonstrates significant therapeutic potential for managing IPTB and enhancing neonatal lung health.
Abstract:
Inflammation-induced preterm birth (PTB) significantly impacts neonatal development, particularly due to fetal lung immaturity. The lungs undergo critical development both in utero and postnatally, and PTB disrupts this process, leading to impaired pulmonary function. Current treatments for promoting lung maturation in preterm infants have limited efficacy and safety. Melatonin, known for its potent antioxidant and anti-inflammatory properties, has shown promise in preventing PTB, but its effects on fetal and postnatal lung maturation remain unclear. This study evaluated the therapeutic efficacy of melatonin in a mouse model of intrauterine inflammation-induced PTB (IPTB). Pregnant mice (Pregnancy Day 17, [PD17]) were assigned to control, lipopolysaccharide (LPS), and LPS + melatonin groups. LPS (25 µg) was injected into the right uterine horn, with melatonin (10 mg/kg) administered intraperitoneally 30 min prior. Uterine tissues were collected at 6 and 24 h post-LPS administration for molecular and histological analyses. PTB occurred in seven out of eleven (63.6%) IPTB mice within 24 h of LPS injection, whereas melatonin significantly reduced this rate to 25% (2/8). In melatonin-treated mice, the downregulation of pro-inflammatory genes in uterine tissues, restoration of placental blood flow, increased lamellar body counts, and prevention of LPS-induced vacuolation in PD18 fetal lungs were observed. Furthermore, melatonin administration enhanced surfactant protein B expression and improved lung structure. In the offspring of IPTB mice that survived, melatonin further suppressed pro-inflammatory markers and promoted lung septal thickening at postnatal day 3. In conclusion, melatonin prevents PTB, mitigates inflammation, and supports fetal lung maturation in IPTB mice, highlighting its therapeutic potential for improving neonatal pulmonary outcomes.
