Solaroglu Ayse, Suat Dede Faruk, Gelisen Orhan, Secilmis Ozlem, Dede Hulya
Etlik Zubeyde Hanim Women's Health Teaching & Research Hospital, Ankara, Turkey.
J Matern Fetal Neonatal Med. 2011 Oct;24(10):1259-61. doi: 10.3109/14767058.2011.572202. Epub 2011 Apr 19.
The aim of this study was to demonstrate the neuroprotective effect of magnesium sulfate on ischemia-reperfusion-induced injury in fetal rat brain.
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.
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.
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.
本研究旨在证明硫酸镁对胎鼠脑缺血再灌注损伤的神经保护作用。
将24只孕19天的大鼠随机分为四组。通过双侧夹闭子宫卵巢动脉20分钟诱导胎脑缺血,松开夹子30分钟实现再灌注。对照组由未受伤的大鼠组成。缺血再灌注组不进行治疗;而在缺血再灌注损伤前30分钟,给溶剂组和治疗组分别注射1毫升生理盐水和600毫克/千克硫酸镁。测定每只胎鼠脑组织中脂质过氧化水平,以硫代巴比妥酸反应性物质(TBARS)的浓度表示。采用单因素方差分析和事后检验进行统计分析。
与对照组相比,缺血再灌注损伤后TBARS水平升高。硫酸镁治疗可防止缺血再灌注损伤后TBARS水平升高。
我们已经表明,硫酸镁可显著降低遭受缺血再灌注损伤的胎鼠脑中TBARS水平,并且通过减少宫内缺血再灌注诱导的胎脑损伤后的氧化应激可能具有潜在的治疗益处。