Melatonin alleviates brain and peripheral tissue edema in a neonatal rat model of hypoxic-ischemic brain damage: the involvement of edema related proteins

Xu, Lixiao; Lv, Yuan; Li, Yanhong; Ding, Xin; Wang, Ying; Han, Xiang; Liu, Minghua; Sun, Bin; Feng, Xing

doi:10.1186/s12887-017-0824-x

Cited by 27 publications

(27 citation statements)

References 35 publications

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“…Hypoxic-ischemic brain injury (HIBI) is a leading cause of mortality and morbidity, which is caused by intrapartum or late antepartum brain hypoxia and ischemia. 1 This potentially devastating event leads to death or long-term neurologic impairment in both adults and children, with fetal distress and hypoxia caused by situations such as the umbilical cord wrapped around the neck. 2 , 3 Despite the recent advances in perinatal care, perinatal hypoxia–ischemia remains a tragic cause of neonatal death and/or severe neurological disorders.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: MicroRNA-132 protects hippocampal neurons against oxygen-glucose deprivation–induced apoptosis

Sun

Tian

et al. 2017

Int J Immunopathol Pharmacol

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Hypoxic-ischemic brain injury (HIBI) results in death or long-term neurologic impairment in both adults and children. In this study, we investigated the effects of microRNA-132 (miR-132) dysregulation on oxygen-glucose deprivation (OGD)-induced apoptosis in fetal rat hippocampal neurons, in order to reveal the therapeutic potential of miR-132 on HIBI. MiR-132 dysregulation was induced prior to OGD exposure by transfection of primary fetal rat hippocampal neurons with miR-132 mimic or miR-132 inhibitor. The effects of miR-132 overexpression and suppression on OGD-stimulated hippocampal neurons were evaluated by detection of cell viability, apoptotic cells rate, and the expression of apoptosis-related proteins. Besides, TargetScan database and dual luciferase activity assay were used to seek a target gene of miR-132. As a result, miR-132 was highly expressed in hippocampal neurons following 2 h of OGD exposure. MiR-132 overexpression significantly increased OGD-diminished cell viability and reduced OGD-induced apoptosis at 12, 24, and 48 h post-OGD. MiR-132 overexpression significantly down-regulated the expressions of Bax, cytochrome c, and caspase-9, but up-regulated BCl-2. Caspase-3 activity was also significantly decreased by miR-132 overexpression. Furthermore, FOXO3 was a direct target of miR-132, and it was negatively regulated by miR-132. To conclude, our results provide evidence that miR-132 protects hippocampal neurons against OGD injury by inhibiting apoptosis.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: MicroRNA-132 protects hippocampal neurons against oxygen-glucose deprivation–induced apoptosis

Sun

Tian

et al. 2017

Int J Immunopathol Pharmacol

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“…In neonatal HIE rats treated with systemic hypothermia, the supplement with N-acetylcysteine reduced the volume of the brain damage at both two weeks and four weeks after the hypoxic–ischemic insult [ 37 ]. Hormones with antioxidative properties, such as melatonin or erythropoietin, displayed neuroprotective properties in HIE models [ 38 , 39 , 40 ]. However, the therapeutic mechanism may include several targets for these substances [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury

et al. 2018

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Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8% oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions. Using vital sections of the brain, SkQR1 has been shown to reduce the development of oxidative stress. Thus, the mitochondrial-targeted antioxidant derived from plant plastoquinone can effectively protect the brain of newborns both in pre-ischemic and post-stroke conditions, making it a promising candidate for further clinical studies.

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“…From our previous studies, we regard this transportation as being a PRL-specific phenomenon. It is known that brain edema generally occurs when the brain falls into a hypoxic condition [ 46 ]. At this point, PRL may transport to CSF from blood, adjust osmotic pressure to the brain, and act on neuroprotection [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Prolactin selectively transported to cerebrospinal fluid from blood under hypoxic/ischemic conditions

et al. 2018

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AimThe aim of this study was to determine and to verify the correlation between the amount of prolactin (PRL) levels in the blood and in the cerebrospinal fluid (CSF) by various causes of death as an indicator for acute hypoxia in autopsy cases. It is to confirm the cause of the change in prolactin level in CSF by in vitro system.Materials and methodsIn autopsy materials, the PRL levels in blood from the right heart ventricle and in the CSF were measured by chemiluminescent enzyme immunoassay, and changes in the percentage of PRL-positive cells in the pituitary gland were examined using an immunohistochemical method. Furthermore, an inverted culture method was used as an in vitro model of the blood-CSF barrier using epithelial cells of the human choroid plexus (HIBCPP cell line) and SDR-P-1D5 or MSH-P3 (PRL-secreting cell line derived from miniature swine hypophysis) under normoxic or hypoxic (5% oxygen) conditions, and as an index of cell activity, we used Vascular Endothelial Growth Factor (VEGF).Results and discussionSerum PRL levels were not significantly different between hypoxia/ischemia cases and other causes of death. However, PRL levels in CSF were three times higher in cases of hypoxia/ischemia than in those of the other causes of death. In the cultured cell under the hypoxia condition, PRL and VEGF showed a high concentration at 10 min. We established a brain-CSF barrier model to clarify the mechanism of PRL transport to CSF from blood, the PRL concentrations from blood to CSF increased under hypoxic conditions from 5 min. These results suggested that PRL moves in CSF through choroidal epithelium from blood within a short time. PRL is hypothesized to protect the hypoxic/ischemic brain, and this may be because of the increased transportation of the choroid plexus epithelial cells.

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Melatonin alleviates brain and peripheral tissue edema in a neonatal rat model of hypoxic-ischemic brain damage: the involvement of edema related proteins

Cited by 27 publications

References 35 publications

RETRACTED: MicroRNA-132 protects hippocampal neurons against oxygen-glucose deprivation–induced apoptosis

RETRACTED: MicroRNA-132 protects hippocampal neurons against oxygen-glucose deprivation–induced apoptosis

Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury

Prolactin selectively transported to cerebrospinal fluid from blood under hypoxic/ischemic conditions

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