Pregnancy swimming causes short- and long-term neuroprotection against hypoxia–ischemia in very immature rats

Sanches, Eduardo Farias; Durán‐Carabali, Luz Elena; Tosta, Andréa; Nicola, Fabrício do Couto; Schmitz, Felipe; Rodrigues, André Felipe; Siebert, Cassiana; Wyse, Ângela T. S.; Netto, Carlos Alexandre

doi:10.1038/pr.2017.110

Cited by 22 publications

(22 citation statements)

References 38 publications

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“…In addition, a region of interest (ROI–19,454 μm 2 ) was drawn on each slice and the staining intensities were quantified in the CA1 area using ImageJ software. Data are expressed as the mean of integrated density value/μm 2 (Sanches et al, 2017).…”

Section: Methodsmentioning

confidence: 99%

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Mari

Odorcyk

Sanches³

et al. 2019

Intl J of Devlp Neuroscience

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Introduction Perinatal hypoxia‐ischemia (HI) is one of the main causes of mortality and chronic neurological morbidity in infants and children. Astrocytes play a key role in HI progression, becoming reactive in response to the injury, releasing S100 calcium binding protein B (S100B). Since S100B inhibition seems to have neuroprotective effects on central nervous system injury models, here we evaluated the neuroprotective effects of an S100B inhibitor, arundic acid (AA) in a HI model. Methods On the 7th postnatal day, animals were submitted to the combination of common carotid artery occlusion and hypoxic atmosphere (8% O2) for 60 min. Three experiments were performed in order to: (1) define AA dose (0.1, 1 or 10 mg/kg, pre‐hypoxia i.p. injection), (2) test if repeated AA administrations (10 mg/kg at 3 time points: Pre‐hypoxia, 24 h and 48 h after HI) would improve the response and (3) investigate biochemical mechanisms involved in AA protection two days after HI. Results AA at a dose of 10 mg/kg applied before and after hypoxia, was the only treatment protocol that was able to improve HI‐induced memory deficits, to reduce tissue damage, to promote astrocytic survival in the hippocampus and to reduced extracellular release of S100B in the cerebrospinal fluid. Conclusion Overall, AA treatment showed beneficial effects on memory deficits, tissue damage, promoting astrocyte survival likely by reducing S100B release. Protection aided to astrocytes by AA treatment against HI lesion may lead to development of new therapeutic strategies that target these particular cells.

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Section: Methodsmentioning

confidence: 99%

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Mari

Odorcyk

Sanches³

et al. 2019

Intl J of Devlp Neuroscience

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“…47 In preclinical studies, maternal exercise during pregnancy was associated with increased BDNF levels and absolute numbers of neuronal and non-neuronal cells in the hippocampus of the adult rat offspring, that was associated with better cognitive performance (habituation behavior and spatial learning). 49 Experimental environmental enrichment has a series of beneficial effects associated with neuroplasticity mechanisms, increasing hippocampal volume, and enhancing dorsal dentate gyrus-specific differences in gene expression. 49 Experimental environmental enrichment has a series of beneficial effects associated with neuroplasticity mechanisms, increasing hippocampal volume, and enhancing dorsal dentate gyrus-specific differences in gene expression.…”

Section: Possible Factors For Reversibilitymentioning

confidence: 99%

Early environmental influences on the development of children's brain structure and function

Miguel

Pereira

Silveira

et al. 2019

Develop Med Child Neuro

194

102

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ABBREVIATION BDNFBrain-derived neurotrophic factorThe developing brain in utero and during the first years of life is highly vulnerable to environmental influences. Experiences occurring during this period permanently modify brain structure and function through epigenetic modifications (alterations of the DNA structure and chromatin function) and consequently affect the susceptibility to mental disorders. In this review, we describe evidence linking adverse environmental variation during early life (from the fetal period to childhood) and long-term changes in brain volume, microstructure, and connectivity, especially in amygdala and hippocampal regions. We also describe genetic variations that moderate the impact of adverse environmental conditions on child neurodevelopment, such as polymorphisms in brain-derived neurotrophic factor and catechol-Omethyltransferase genes, as well as genetic pathways related to glutamate and monoaminergic signaling. Lastly, we have depicted positive early life experiences that could benefit childhood neurodevelopment and reverse some detrimental effects of adversity in the offspring.

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“…HI rats show cognitive disabilities, with males being more susceptible to tissue loss in structure such as the CA1 area of hippocampus, a critical region for cognitive tasks (Arteni et al, 2010; Dai et al, 2017; Netto et al, 2017). Long‐term assessment of cognitive impairment, at 60 postnatal days and 90 postnatal days, has been reported after experimental neonatal HI (Arteaga et al, 2015; Sanches et al, 2017). However, there are no reports in the literature showing the beneficial effects of coumestrol treatment against the late cognitive deficits induced by neonatal HI model.…”

Section: Discussionmentioning

confidence: 99%

Phytoestrogen coumestrol attenuates brain mitochondrial dysfunction and long‐term cognitive deficits following neonatal hypoxia–ischemia

Anastácio

Sanches

Nicola

et al. 2019

Intl J of Devlp Neuroscience

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Introduction: Neonatal Hypoxia-Ischemia (HI) is a major cause of morbidity and mortality, and is frequently associated with short and long-term neurologic and cognitive impairments. The HI injury causes mitochondrial damage leading to increased production of reactive oxygen species (ROS). Phytoestrogens are non-steroidal plant substances structurally and functionally similar to estrogen. Coumestrol is a potent isolavonoid with a protective efect against ischemic brain damage in adult rats. Our aim was to determine if coumestrol treatment following neonatal HI attenuates the long-term cognitive deicits induced by neonatal HI, as well as to investigate one possible mechanism underlying its potential efect. Methods: On the 7th postnatal day, male Wistar rats were submitted to the Levine-Rice HI model. Intraperitoneal injections of 20 mg/kg of coumestrol, or vehicle, were administered immediately pre-hypoxia or 3 h post-hypoxia. At 12 h after HI the mitochondrial status and ROS levels were determined. At 60th postnatal day the cognitive deicits were revealed in the Morris water maze reference and working spatial memories. Following behavioral analysis, histological assessment was performed and reactive astrogliosis was measured by GFAP expression. Results: Results demonstrate that both pre-and post-HI administration of coumestrol were able to counteract the long-term cognitive and morphological impairments caused by HI, as well as to block the late reactive astrogliosis. The pre-HI administration of coumestrol was able to prevent the early mitochondrial dysfunction in the hippocampus of injured rat pups. Conclusion: Present data suggest that coumestrol exerts protection against experimental neonatal brain hypoxiaischemia through, at least in part, early modulation of mitochondrial function.

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Pregnancy swimming causes short- and long-term neuroprotection against hypoxia–ischemia in very immature rats

Cited by 22 publications

References 38 publications

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Early environmental influences on the development of children's brain structure and function

Phytoestrogen coumestrol attenuates brain mitochondrial dysfunction and long‐term cognitive deficits following neonatal hypoxia–ischemia

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