Melatonin modulates neonatal brain inflammation through endoplasmic reticulum stress, autophagy, and mi R ‐34a/silent information regulator 1 pathway
Open accessAbstract
Maternal infection/inflammation represents one of the most important factors involved in the etiology of brain injury in newborns. We investigated the modulating effect of prenatal melatonin on the neonatal brain inflammation process resulting from maternal intraperitoneal (i.p.) lipopolysaccharide ( LPS ) injections. LPS (300 μg/kg) was administered to pregnant rats at gestational days 19 and 20. Melatonin (5 mg/kg) was administered i.p. at the same time as LPS . Melatonin counteracted the LPS sensitization to a second ibotenate‐induced excitotoxic insult performed on postnatal day ( PND ) 4. As melatonin succeeded in reducing microglial activation in neonatal brain at PND 1, pathways previously implicated in brain inflammation regulation, such as endoplasmic reticulum ( ER ) stress, autophagy and silent information regulator 1 ( SIRT 1), a melatonin target, were assessed at the same time‐point in our experimental groups. Results showed that maternal LPS administrations resulted in an increase in CHOP and Hsp70 protein expression and eIF 2α phosphorylation, indicative of activation of the unfolded protein response consequent to ER stress, and a slighter decrease in the autophagy process, determined by reduced lipidated LC 3 and increased p62 expression. LPS ‐induced inflammation also reduced brain SIRT 1 expression and affected the expression of miR‐34a, miR146a, and miR‐126. All these effects were blocked by melatonin. Cleaved‐caspase‐3 apoptosis pathway did not seem to be implicated in the noxious effect of LPS on the PND 1 brain. We conclude that melatonin is effective in reducing maternal LPS ‐induced neonatal inflammation and related brain injury. Its role as a prophylactic/therapeutic drug deserves to be investigated by clinical studies.
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Maternal LPS exposure reduces miR-126 and miR-146 in the whole brain of PND1 rats.
“In the whole brain of PND1 rats (sex undeclared) subject to maternal LPS exposure 48 h earlier, there was reduced miR-126 and miR-146 [132], which regulate microglial inflammatory processes [107].”
From Cell-type-specific epigenetic effects of early life stress on the brain (2022) · cites this paper as [132]
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- Authors
- Carloni, S., Favrais, G., Saliba, E., Albertini, M. C., Chalon, S., Longini, M., Gressens, P., Buonocore, G., & Balduini, W.
- Affiliations
- University of Urbino (IT)
- Université de Tours (FR)
- Department of Neonatal and Pediatric Intensive Care CHRU de Tours Tours France
- University of Siena (IT)
- PROTECT INSERM Université Paris Diderot Sorbonne Paris Cité Paris France
- Corresponding author
- Balduini, Walter
- ORCID
- Venue
- Journal of Pineal Research
- Publisher
- Wiley
- Published
- 2016-08-13
- Volume
- 61
- Issue
- 3
- Pages
- 370-380
- ISSN
- 0742-3098 (ISSN-L)
- 1600-079X
- OpenAlex
- W2495998807
- Cited by
- 124
- References
- 70
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 10 · 2023: 12 · 2022: 12 · 2021: 15 · 2020: 11 · 2019: 17 · 2018: 23 · 2017: 12 · 2016: 3
- FWCI
- 21.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Pineal Research (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (publishedVersion, other-oa)
- CINECA IRIS Institutional Research information system (University of Urbino) (submittedVersion, cc-by-nc-nd)
- Use Siena air (University of Siena) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- melatonin, endoplasmic reticulum stress, autophagy, SIRT1, miR-34a, microglial activation, excitotoxicity, ibotenate, unfolded protein response, CHOP, HSP70, eIF2α phosphorylation, LC3, p62, neuroprotection, perinatal brain injury
- MeSH terms
- Animals, Animals, Newborn, Autophagy, Brain, Female, Inflammation, Lipopolysaccharides, Melatonin, Nerve Tissue Proteins, Pregnancy, Prenatal Exposure Delayed Effects, Signal Transduction, Rats, Wistar, MicroRNAs, Rats, Endoplasmic Reticulum Stress
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