Journal of neuroscience research · 2012
Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Goñi-de-Cerio Felipe, Alvarez Antonia, Lara-Celador Idoia, Alvarez Francisco J, Alonso-Alconada Daniel, Hilario Enrique
Аннотация
The aim of this work was to analyze the effect of MgSO(4) treatment in the brain after hypoxic-ischemic (HI) injury in premature fetal lambs. Injury was induced by partial occlusion of umbilical cord for 60 min, and then the preterm lambs (80-90% of gestation) were randomly assigned to one of the following groups: control group, in which the animals were managed by conventional mechanical ventilation for 3 hr; 3 hr postpartial cord occlusion (3-hr-PCO) group, in which injured animals were managed by ventilation and then sacrificed 3 hr after HI; and MgSO(4) group, in which animals received 400 mg/kg MgSO(4) for 20 min soon after HI was induced and were managed by ventilation for 3 hr. Brains were analyzed for apoptosis by TUNEL assay. Cell viability and intracellular state studies were assessed by flow cytometry. The delayed death index was significantly increased in the 3-hr-PCO group in comparison with control. Administration of MgSO(4) elicited a delay in cell death that was similar to that in the control group. The 3-hr-PCO group showed a significantly higher concentration of reactive oxygen species, mitochondrial damage, and intracellular calcium in comparison with control and MgSO(4) - treated groups. Our results suggest that MgSO(4) treatment might have potential therapeutic benefits after the HI event.
Предметные рубрики MeSH
AnimalsAnimals, NewbornAnnexin A5ApoptosisAsphyxiaBrain Damage, ChronicCalciumCarotid ArteriesCell MembraneFemaleFetusFluorescent DyesImmunohistochemistryIn Situ Nick-End LabelingMagnesium SulfateMembrane PotentialsMitochondrial MembranesPregnancyPrimed In Situ LabelingReactive Oxygen SpeciesRhodamine 123SheepSpinal Cord