The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2011
Neuroprotective effect of magnesium sulfate treatment on fetal brain in experimental intrauterine ischemia reperfusion injury.
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Solaroglu Ayse, Suat Dede Faruk, Gelisen Orhan, Secilmis Ozlem, Dede Hulya
Аннотация
OBJECTIVE: The aim of this study was to demonstrate the neuroprotective effect of magnesium sulfate on ischemia-reperfusion-induced injury in fetal rat brain.
METHODS: Twenty-four, 19-days pregnant rats were randomly allocated into four groups. Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 20 min and reperfusion was achieved by removing the clamps for 30 min. The control group consisted of noninjured rats. No treatment was given in the ischemia-reperfusion group; whereas 1 ml saline and 600 mg/kg magnesium sulfate was administered in the vehicle and the treatment groups 30 min before ischemia reperfusion injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each fetal rat. A one-way analysis of variance and post hoc test were used for statistical analysis.
RESULTS: TBARS levels were found to be increased after ischemia reperfusion injury when compared with controls. Magnesium sulfate treatment prevented the increase in TBARS after ischemia reperfusion injury.
CONCLUSIONS: 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.
METHODS: Twenty-four, 19-days pregnant rats were randomly allocated into four groups. Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 20 min and reperfusion was achieved by removing the clamps for 30 min. The control group consisted of noninjured rats. No treatment was given in the ischemia-reperfusion group; whereas 1 ml saline and 600 mg/kg magnesium sulfate was administered in the vehicle and the treatment groups 30 min before ischemia reperfusion injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each fetal rat. A one-way analysis of variance and post hoc test were used for statistical analysis.
RESULTS: TBARS levels were found to be increased after ischemia reperfusion injury when compared with controls. Magnesium sulfate treatment prevented the increase in TBARS after ischemia reperfusion injury.
CONCLUSIONS: 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.