Glial cell survival is enhanced during melatonin-induced neuroprotection against cerebral ischemia

Borlongan, Cesario V.; Yamamoto, Mitsuharu; Takei, Norie; Kumazaki, Michiko; Ungsuparkorn, Chutcharin; Hida, Hideki; Sanberg, Paul R.; Nishino, Hitoo

doi:10.1096/fj.14.10.1307

Cited by 121 publications

(85 citation statements)

References 65 publications

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“…This might be a compensatory mechanism for neuronal damage caused by Bisphenol A. These changes have been proved previously in other forms of neurotoxicity [29] .…”

Section: Discussionsupporting

confidence: 65%

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

Elaziz

Laag

2018

Egyptian Journal of Histology

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Introduction: Bisphenol A (BPA), a well-known industrial chemical, has adverse effects on the brain even at relatively low exposure levels in rodents, primates and humans. Omega-3-fatty acids participate in a number of neuronal processes including neurogenesis, neuron differentiation, and neuro-protection. Aim of the work: To investigate the possible protective action of omega-3-fatty acids on the injurious histological effect induced by Bisphenol A on rat hippocampus. Materials and Methods: Eighteen adult male Wistar rats were divided into 3 equal groups; control, BPA (1.2mg/kg daily for 3 weeks, intraperitoneally) and the third group were given omega-3 (300mg/kg orally) in addition to BPA in the aforementioned dose and duration. Hippocampus sections were processed for hematoxylin and eosin staining, GFAB staining and electron microscopic examination. Results: BBPA administration resulted into several histological alterations. Glial fibrillary acidic protein-positive cells were more abundant in the hippocampus of BPA-treated animals compared with the control animals. Ultra-structurally, the hippocampus of BPA-treated group showed nerve cells having nuclei with irregular outline and dilated perinuclear envelop, dilated RER and Golgi, swollen mitochondria with destroyed cristae. Some of the myelinated and unmyelinated nerve fibers showed degenerative changes. Concomitant administration of omega-3-fatty acids ameliorated these effects. Conclusions: OOmega-3-fatty acids partially minimized the severity of BPA-induced hippocampus injurious histological effects in Wistar rat.

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“…This might be a compensatory mechanism for neuronal damage caused by Bisphenol A. These changes have been proved previously in other forms of neurotoxicity [29] .…”

Section: Discussionsupporting

confidence: 65%

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

Elaziz

Laag

2018

Egyptian Journal of Histology

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“…Endogenous melatonin was found protective (9), and there is compelling in vivo and in vitro evidence supporting the use of exogenous melatonin to protect against focal and global ischemia-reperfusion injury in adult animals (25)(26)(27)(28). Pretreatment with a single dose significantly reduces the infarct volume by ϳ40% without affecting the hemodynamic parameters and regional cerebral blood flow (10).…”

Section: Discussionmentioning

confidence: 99%

Melatonin Promotes Myelination by Decreasing White Matter Inflammation After Neonatal Stroke

et al. 2011

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Melatonin demonstrates neuroprotective properties in adult models of cerebral ischemia, acting as a potent antioxidant and anti-inflammatory agent. We investigated the effect of melatonin in a 7-d-old rat model of ischemia-reperfusion, leading to both cortical infarct and injury in the underlying white matter observed using MRI and immunohistochemistry. Melatonin was given i.p. as either a single dose before ischemia or a double-dose regimen, combining one before ischemia and one 24 h after reperfusion. At 48 h after injury, neither a significant reduction in cortical infarct volume nor a variation in the number of TUNEL-and nitrotyrosine-positive cells within the ipsilateral lesion was observed in melatonin-treated animals compared with controls. However, a decrease in the density of tomato lectin-positive cells after melatonin treatment was found in the white matter underlying cortical lesion. Furthermore, we showed a marked increase in the myelin basic protein-immunoreactivity in the cingulum and in the density of mature oligodendrocytes (APCimmunoreactive) in both the ipsilateral cingulum and external capsule. These results suggest that melatonin is not able to reduce cortical infarct volume in a neonatal stroke model but strongly reduces inflammation and promotes subsequent myelination in the white matter. (Pediatr Res 69: 51-55, 2011) N eonatal hypoxia-ischemia is an important cause of neonatal brain injury, resulting in cerebral palsy, learning disabilities, visual field deficits, and epilepsy (1). In addition to global cerebral ischemia arising from systemic asphyxia, recent data suggest a higher incidence of focal ischemiareperfusion leading to stroke in near-term neonates (2,3). Mechanisms of arterial ischemic injury without the confounding effect of hypoxia are not fully understood. Although therapeutic hypothermia has recently demonstrated a benefit by decreasing brain tissue injury in infants with hypoxicischemic encephalopathy (4,5), very little is known regarding potential neuroprotective strategies after neonatal stroke.Melatonin, an indoleamine, is synthesized and secreted from the pineal gland relative to the circadian rhythms. Melatonin readily crosses the blood-brain barrier, and after exogenous administration, it is found in high concentrations in the brain. It was demonstrated that melatonin has neuroprotective effects through either antiapoptotic (6) or antioxidant effects (7,8) or by decreasing the excitotoxic cascade (9). Melatonin has demonstrated neuroprotective properties in adult models of cerebral ischemia, acting as a potent antioxidant and antiinflammatory agent (10,11). Melatonin was shown to have a potent protective effect in several models of developing white matter damage, by not only promoting oligodendroglial maturation and myelination repair but also decreasing astrogliosis and microglial activation (12-15). We previously developed a neonatal model of stroke in 7-d-old (P7) rat characterized by apoptotic cell death (16,17), inflammatory responses (18,19), and oxid...

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“…After staining, the sections were mounted in hardset vectashield medium containing DAPI. Additional staining was done with hematoxylin-eosin to locate the boundary of ischemic penumbra (28). The sections were photographed using a fluorescence microscope equipped with AxioVision software.…”

Section: Methodsmentioning

confidence: 99%

Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice

Canugovi

Yoon

Feldman

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Recent findings suggest that neurons can efficiently repair oxidatively damaged DNA, and that both DNA damage and repair are enhanced by activation of excitatory glutamate receptors. However, in pathological conditions such as ischemic stroke, excessive DNA damage can trigger the death of neurons. Oxidative DNA damage is mainly repaired by base excision repair (BER), a process initiated by DNA glycosylases that recognize and remove damaged DNA bases. Endonuclease VIII-like 1 (NEIL1) is a DNA glycosylase that recognizes a broad range of oxidative lesions. Here, we show that mice lacking NEIL1 exhibit impaired memory retention in a water maze test, but no abnormalities in tests of motor performance, anxiety, or fear conditioning. NEIL1 deficiency results in increased brain damage and a defective functional outcome in a focal ischemia/reperfusion model of stroke. The incision capacity on a 5-hydroxyuracil-containing bubble substrate was lower in the ipsilateral side of ischemic brains and in the mitochondrial lysates of unstressed old NEIL1-deficient mice. These results indicate that NEIL1 plays an important role in learning and memory and in protection of neurons against ischemic injury. Increased oxidative stress and decreased DNA repair occur during normal brain aging and in disorders in which neurons degenerate, including stroke (1) and Alzheimer's disease (2, 3). Neuronal cells encounter relatively more oxidative DNA damage due to their high metabolic rate, which is necessary for maintaining their electrochemical signaling functions. Reactive oxygen species generated as a byproduct of metabolic activities can create oxidative DNA lesions in addition to damage to other cellular constituents. Unrepaired oxidative DNA lesions can cause detrimental effects to the cell, including dysregulation of gene expression and cell death. The integrity of DNA repair systems is therefore presumed to be an important prerequisite for proper brain function and oxidative stress resistance.Oxidative DNA damage is repaired mainly by the base excision repair (BER) system (4). BER is initiated by a DNA glycosylase that recognizes and removes the damaged base. This activity is followed by an endonuclease to process the abasic site, and then a DNA polymerase completes gap filling. The reaction is completed by the activity of a DNA ligase, which seals the nick. Although there are 11 known DNA glycosylases in higher vertebrates, oxidative base lesions are mainly removed by 8-oxoguanine DNA glycosylase 1 (OGG1), endonuclease III like-1 (NTH1), and endonuclease VIII-like (NEIL) family members (NEIL1, -2, and -3) (5).NEIL1 is a versatile DNA repair enzyme as it has a broad range and overlapping substrate specificity with other DNA glycosylases. NEIL1 can efficiently recognize and remove 5-hydroxyuracil, 5-hydroxycytosine, thymine glycol, and formamidopyrimidine (FAPY) lesions (5). NEIL1 also participates in interstrand cross-link repair and nucleotide excision repair in addition to BER (6, 7). NEIL1 activity is stimulated by physical and fun...

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Glial cell survival is enhanced during melatonin-induced neuroprotection against cerebral ischemia

Cited by 121 publications

References 65 publications

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

Melatonin Promotes Myelination by Decreasing White Matter Inflammation After Neonatal Stroke

Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice

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