Cited by 124Neonatal and fetal brain pathologyNeuroinflammation and Neurodegeneration MechanismsCircadian rhythm and melatonin

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Melatonin modulates neonatal brain inflammation through endoplasmic reticulum stress, autophagy, and mi R ‐34a/silent information regulator 1 pathway

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Carloni, Silvia, Favrais, Géraldine, Saliba, Elie, Albertini, Maria Cristina, Chalon, Sylvie, Longini, Mariangela, Gressens, Pierre, Buonocore, Giuseppe, Balduini, Walter·2016·Journal of Pineal Research

DOI 10.1111/jpi.12354

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Abstract

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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Self-citation
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RETRACTED: CircSEC11A knockdown alleviates oxidative stress and apoptosis and promotes cell proliferation and angiogenesis by regulating miR-29a-3p/SEMA3A axis in OGD-induced human brain microvascular endothelial cells (HBMECs)
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Retracted
Maternal Prenatal Inflammation Increases Brain Damage Susceptibility of Lipopolysaccharide in Adult Rat Offspring via COX-2/PGD-2/DPs Pathway Activation
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Sudden infant death syndrome: Melatonin, serotonin, and CD34 factor as possible diagnostic markers and prophylactic targets
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Retracted
Analysis of miRNA expression profiles in melatonin-exposed GC-1 spg cell line
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Fine particulate matter‑induced cardiac developmental toxicity (Review)
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Noncoding RNAs: Bridging Regulation of Circadian Rhythms and Inflammation
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Melatonin attenuates cardiopulmonary toxicity induced by benzo(a)pyrene in mice focusing on apoptosis and autophagy pathways
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On the Relationships between LncRNAs and Other Orchestrating Regulators: Role of the Circadian System
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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: Carloni, Silvia
Favrais, Géraldine
Albertini, Maria Cristina
Chalon, Sylvie
Longini, Mariangela
Buonocore, Giuseppe
Balduini, Walter
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
DOI: 10.1111/jpi.12354
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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Melatonin modulates neonatal brain inflammation through endoplasmic reticulum stress, autophagy, and mi R ‐34a/silent information regulator 1 pathway

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