Melatonin utility in neonates and children

Chen, Yu-Chieh; Tain, You‐Lin; Sheen, Jiunn‐Ming; Huang, Laura

doi:10.1016/j.jfma.2011.11.024

Cited by 67 publications

(57 citation statements)

References 100 publications

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“…In this study, we found that melatonin restored the levels of hippocampal reln mRNA expression by reducing DNMT1 and MeCP2 binding to the reln promoter. Melatonin has been used in treating compromised pregnancies, including those affected by prenatal stress [23,24]. In our study, we found that melatonin restored the levels of hippocampal reln mRNA expression by reducing DNMT1 and MeCP2 binding to the reln promoter.…”

Section: Discussionsupporting

confidence: 57%

“…Due to its antioxidant properties, it might improve quality of life, reduce healthcare costs, and help reduce complications in the neonatal period [23]. Recently, a study showed that agomelatine, which is a mixed melatonin-1 and -2 receptor/serotonin receptor antagonist, corrects many aspects of pathological epigenetic programming triggered by prenatal stress [24].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Melatonin on Prenatal Dexamethasone-Induced Epigenetic Alterations in Hippocampal Morphology and Reelin and Glutamic Acid Decarboxylase 67 Levels

et al. 2015

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Prenatal glucocorticoid exposure causes brain damage in adult offspring; however, the underlying mechanisms remain unclear. Melatonin has been shown to have beneficial effects in compromised pregnancies. Pregnant Sprague-Dawley rats were administered vehicle (VEH) or dexamethasone between gestation days 14 and 21. The programming effects of prenatal dexamethasone exposure on the brain were assessed at postnatal days (PND) 7, 42, and ∼120. Melatonin was administered from PND21 to the rats exposed to dexamethasone, and the outcome was assessed at ∼PND120. In total, there were four groups: VEH, vehicle plus melatonin (VEHM), prenatal dexamethasone-exposure (DEX), and prenatal dexamethasone exposure plus melatonin (DEXM). Spatial memory, gross hippocampal morphology, and hippocampal biochemistry were examined. Spatial memory assessed by the Morris water maze showed no significant differences among the four groups. Brain magnetic resonance imaging showed that all rats with prenatal dexamethasone exposure (DEX + DEXM) exhibited increased T2-weighted signals in the hippocampus. There were no significant differences in the levels of mRNA expression of hippocampal reln, which encodes reelin, and GAD1, which encodes glutamic acid decarboxylase 67, at PND7. At both PND42 and ∼PND120, reln and GAD1 mRNA expression levels were decreased. At ∼PND120, melatonin restored the reduced levels of hippocampal reln and GAD1 mRNA expression in the DEXM group. In addition, melatonin restored the reln mRNA expression levels by (1) reducing DNA methyltransferase 1 (DNMT1) mRNA expression and (2) reducing the binding of DNMT1 and the methyl-CpG binding protein 2 (MeCP2) to the reln promoter. The present study showed that prenatal dexamethasone exposure induced gross alterations in hippocampal morphology and reduced the levels of hippocampal mRNA expression of reln and GAD1. Spatial memory was unimpaired. Thus, melatonin had a beneficial effect in restoring hippocampal reln mRNA expression by reducing DNMT1 and MeCP2 binding to the reln promoter.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Effects of Melatonin on Prenatal Dexamethasone-Induced Epigenetic Alterations in Hippocampal Morphology and Reelin and Glutamic Acid Decarboxylase 67 Levels

et al. 2015

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“…6 Following birth its production has been suggested to have a role in brain development and pineal dysfunction was associated with sudden infant death. 7,8 Melatonin supplementation has been studied in adults, children and neonates. It was studied in neonates with respiratory distress syndrome, 9 sepsis 10 and as a preoperative antioxidant.…”

Section: Introductionmentioning

confidence: 99%

Melatonin use for neuroprotection in perinatal asphyxia: a randomized controlled pilot study

et al. 2014

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“…Clinically, melatonin has been used in pediatrics to treat respiratory distress syndrome, bronchopulmonary dysplasia, seizure disorders and to reduce oxidative stress in sepsis and asphyxia (Gitto et al, 2011, Sanchez-Barcelo et al, 2011, Aversa et al, 2012, Chen et al, 2012). Thus, melatonin may potentially protect against brain injury induced by infection or inflammation, by attenuating the induction of nitrosative and oxidative stress in neonates.…”

Section: Introductionmentioning

confidence: 99%

Melatonin ameliorates brain injury induced by systemic lipopolysaccharide in neonatal rats

et al. 2014

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Our previous study showed that lipopolysaccharide (LPS)-induced brain injury in the neonatal rat is associated with nitrosative and oxidative stress. The present study was conducted to examine whether melatonin, an endogenous molecule with antioxidant properties, reduces systemic LPS-induced nitrosative and oxidative damage in the neonatal rat brain. Intraperitoneal (i.p.) injection of LPS (2 mg/kg) was administered to Sprague–Dawley rat pups on postnatal day 5 (P5), and i.p. administration of melatonin (20 mg/kg) or vehicle was performed 5 minutes after LPS injection. Sensorimotor behavioral tests were performed 24 h after LPS exposure, and brain injury was examined after these tests. The results show that systemic LPS exposure resulted in impaired sensorimotor behavioral performance, and acute brain injury, as indicated by the loss of oligodendrocyte immunoreactivity and a decrease in mitochondrial activity in the neonatal rat brain. Melatonin treatment significantly reduced LPS-induced neurobehavioral disturbances and brain damage in neonatal rats. The neuroprotective effect of melatonin was associated with attenuation of LPS-induced nitrosative and oxidative stress, as indicated by the decreased nitrotyrosine- and 4-hydroxynonenal-positive staining in the brain following melatonin and LPS exposure in neonatal rats. Further, melatonin significantly attenuated LPS-induced increases in the number of activated microglia in the neonatal rat brain. The protection provided by melatonin was also associated with a reduced number of inducible nitric oxide synthase (iNOS)+ cells, which were double-labeled with ED1 (microglia). Our results show that melatonin prevents the brain injury and neurobehavioral disturbances induced by systemic LPS exposure in neonatal rats, and its neuroprotective effects are associated with its impact on nitrosative and oxidative stress.

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Melatonin utility in neonates and children

Cited by 67 publications

References 100 publications

Effects of Melatonin on Prenatal Dexamethasone-Induced Epigenetic Alterations in Hippocampal Morphology and Reelin and Glutamic Acid Decarboxylase 67 Levels

Effects of Melatonin on Prenatal Dexamethasone-Induced Epigenetic Alterations in Hippocampal Morphology and Reelin and Glutamic Acid Decarboxylase 67 Levels

Melatonin use for neuroprotection in perinatal asphyxia: a randomized controlled pilot study

Melatonin ameliorates brain injury induced by systemic lipopolysaccharide in neonatal rats

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