Neuroprotective effect of magnesium sulfate treatment on fetal brain in experimental intrauterine ischemia reperfusion injury

Solaroglu, Ayse; Dede, Suat; Gelişen, Orhan; Secilmis, Ozlem; Dede, Hülya

doi:10.3109/14767058.2011.572202

Cited by 8 publications

(4 citation statements)

References 33 publications

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“…The protective efficacy of magnesium in permanent as well as in transient ischemia varies widely among the different studies reported. Thus, magnesium has been demonstrated to have protective effects in some animal models of brain damage in neonates (Mami et al,2006; Spandou et al,2007; Solaroglu et al,2011). Magnesium sulfate has also been shown to decrease the magnitude of the lesions in other animal models of focal hypoxic–ischemic and excytotoxic brain lesions (Marret et al,2007; Kang et al,2011).…”

Section: Discussionmentioning

confidence: 99%

“…These paradoxical perspectives regarding the neuroprotective effect of MgSO 4 administration could be the consequence of variability in study design, depending on the dose and the experimental model, making it difficult to compare the outcomes directly. Studies with newborn rodents and different magnesium doses presented divergent results, including neuroprotection (Zhu et al, 2005;Spandou et al, 2007;Pazaiti et al, 2009;Cetinkaya et al, 2010;Solaroglu et al, 2011;Kang et al, 2011) or its absence (Greenwood et al, 2000;Gee et al, 2004;Zhu et al, 2004;Westermaier et al, 2005;Kalincik and Maresova, 2005;Dribben et al, 2009). On the other hand, although lamb or pig models are closer to humans (Yager, 2004), to date there are few studies on the protective effect of MgSO 4 administration in these newborn mammals suffering neonatal HI encephalopathy.…”

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confidence: 99%

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Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs

Goñi‐de‐Cerio¹,

Álvarez²,

Lara-Celador³

et al. 2012

J of Neuroscience Research

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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.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs

Goñi‐de‐Cerio¹,

Álvarez²,

Lara-Celador³

et al. 2012

J of Neuroscience Research

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“…In addition, MgSO4 pretreatment was able to reduce hypoxia effects in genes related to cell cycle, mitochondrial activity, cell death and neurogenesis in cerebellum (Haramati et al, 2010) and has also shown beneficial effects on the brain injury and body weight 72 h after severe maternal hypoxia (Hallak et al, 2000). MgSO 4 , used as a preventive treatment, has anti‐oxidant properties in a model of maternal hypoxia by reducing free radicals overproduction in term fetuses brains of guinea pigs (Maulik et al, 1999), and decreases lipid peroxidation 30 min after reperfusion following bilateral occlusion of utero‐ovarian arteries in rats (Solaroglu et al, 2011). In a similar model, maternal MgSO 4 treatment associated to dexamethasone reduced lipid peroxidation and mitochondrial damage induced by transient occlusion of utero‐ovarian arteries 60 min after reperfusion (Hasturk et al, 2013).…”

Section: Pharmacological Agentsmentioning

confidence: 99%

Pregnancy as a valuable period for preventing hypoxia‐ischemia brain damage

Netto

Sanches

Odorcyk

et al. 2018

Intl J of Devlp Neuroscience

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Neonatal brain Hypoxia-Ischemia (HI) is one of the major causes of infant mortality and lifelong neurological disabilities. The knowledge about the physiopathological mechanisms involved in HI lesion have increased in recent years, however these findings have not been translated into clinical practice. Current therapeutic approaches remain limited; hypothermia, used only in term or near-term infants, is the golden standard. Epidemiological evidence shows a link between adverse prenatal conditions and increased risk for diseases, health problems, and psychological outcomes later in life, what makes pregnancy a relevant period for preventing future brain injury. Here, we review experimental literature regarding preventive interventions used during pregnancy, i.e., previous to the HI injury, encompassing pharmacological, nutritional and/or behavioral strategies. Literature review used PubMed database. A total of forty one studies reported protective properties of maternal treatments preventing perinatal hypoxia-ischemia injury in rodents. Pharmacological agents and dietary supplementation showed mainly anti-excitotoxicity, anti-oxidant or anti-apoptotic properties. Interestingly, maternal preconditioning, physical exercise and environmental enrichment seem to engage the same referred mechanisms in order to protect neonatal brain against injury. This construct must be challenged by further studies to clearly define the main mechanisms responsible for neuroprotection to be explored in experimental context, as well as to test their potential in clinical settings.

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“…These paradoxical perspectives regarding the neuroprotective effect of MgSO 4 administration could be the consequence of the variability in the study design, depending on the dose and the experimental model, making it difficult to compare the outcomes directly. Studies with newborn rodents and different magnesium doses presented divergent results, including neuroprotection [125,126,127,128,129,130] or its absence [115,131,132,133,134,135]. On the other hand, although lamb or pig models are closer to humans [136], up to date there are few studies on the protective effect of MgSO 4 administration in these newborn mammals suffering neonatal HI encephalopathy [114].…”

Section: Pharmacological Therapiesmentioning

confidence: 99%

Neuroprotective Therapies after Perinatal Hypoxic-Ischemic Brain Injury

et al. 2013

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Hypoxic-ischemic (HI) brain injury is one of the main causes of disabilities in term-born infants. It is the result of a deprivation of oxygen and glucose in the neural tissue. As one of the most important causes of brain damage in the newborn period, the neonatal HI event is a devastating condition that can lead to long-term neurological deficits or even death. The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later. Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time. Due to difficulties regarding the early diagnosis and treatment of HI injury, there is an increasing need to find effective therapies as new opportunities for the reduction of brain damage and its long term effects. Some of these therapies are focused on prevention of the production of reactive oxygen species, anti-inflammatory effects, anti-apoptotic interventions and in a later stage, the stimulation of neurotrophic properties in the neonatal brain which could be targeted to promote neuronal and oligodendrocyte regeneration.

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Neuroprotective effect of magnesium sulfate treatment on fetal brain in experimental intrauterine ischemia reperfusion injury

Abstract: We have shown that magnesium sulfate decreases TBARS levels significantly in fetal rat brain subjected to ischemia reperfusion injury and may have potential therapeutic benefits by reducing oxidative stress after intrauterine ischemia-reperfusion-induced fetal brain damage.

Cited by 8 publications

References 33 publications

Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs

Magnesium sulfate treatment decreases the initial brain damage alterations produced after perinatal asphyxia in fetal lambs

Pregnancy as a valuable period for preventing hypoxia‐ischemia brain damage

Neuroprotective Therapies after Perinatal Hypoxic-Ischemic Brain Injury

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