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大鼠皮质注射氯化铁后的脂质过氧化和谷胱甘肽水平:曲美他嗪和去铁胺的作用

Lipid peroxidation and glutathione levels after cortical injection of ferric chloride in rats: effect of trimetazidine and deferoxamine.

作者信息

Suzer T, Coskun E, Demir S, Tahta K

机构信息

Department of Neurosurgery, Pamukkale University School of Medicine, Denizli, Turkey.

出版信息

Res Exp Med (Berl). 2000 Feb;199(4):223-9.

PMID:10743680
Abstract

Intracortical injection of iron salts causes seizures. Oxidation of lipids in neural membranes by reactive oxygen species is involved in the mechanism responsible for iron-induced seizures as a model of posttraumatic epilepsy. In this study, we examined the effect of trimetazidine (TMZ) and deferoxamine (DFO) on lipid peroxidation after cortical injection of 5 microliters of an aqueous solution containing 100 mM of ferric chloride (FeCl3) in rats. Animals were divided into four groups (n = 7 each) and treated as follows: group 1, saline injection into the cortex (control group); group 2, iron injection into the cortex (injury group); group 3, iron injection into the cortex plus TMZ; group 4, iron injection into the cortex plus DFO. The animals were killed 3 h after injections, and the levels of malondialdehyde (MDA), a lipid peroxidation product, and reduced glutathione (GSH) were measured. A significant elevation of MDA was observed in group 2 (P < 0.05). MDA levels were found to be lower in both the TMZ-treated (P < 0.05) and DFO-treated (P < 0.05) groups than in the injury group. Tissue GSH levels were significantly decreased in group 2 (P < 0.05). GSH levels were increased in the TMZ-treated (P < 0.05) and DFO-treated (P < 0.05) groups compared to the injury group. The results of our study suggest that lipid peroxidation is a critical event in iron-induced epilepsy and that treatment with TMZ and DFO is effective in preventing the formation of free radicals and reducing lipoperoxides in brain tissue.

摘要

皮质内注射铁盐会引发癫痫发作。活性氧对神经细胞膜脂质的氧化作用参与了铁诱导癫痫发作的机制,这是创伤后癫痫的一种模型。在本研究中,我们检测了曲美他嗪(TMZ)和去铁胺(DFO)对大鼠皮质注射5微升含100 mM氯化铁(FeCl3)水溶液后脂质过氧化的影响。将动物分为四组(每组n = 7),并进行如下处理:第1组,向皮质注射生理盐水(对照组);第2组,向皮质注射铁(损伤组);第3组,向皮质注射铁加TMZ;第4组,向皮质注射铁加DFO。注射后3小时处死动物,测量脂质过氧化产物丙二醛(MDA)和还原型谷胱甘肽(GSH)的水平。第2组MDA显著升高(P < 0.05)。发现TMZ处理组(P < 0.05)和DFO处理组的MDA水平均低于损伤组。第2组组织GSH水平显著降低(P < 0.05)。与损伤组相比,TMZ处理组(P < 0.05)和DFO处理组的GSH水平升高。我们的研究结果表明,脂质过氧化是铁诱导癫痫中的关键事件,TMZ和DFO治疗可有效预防自由基形成并减少脑组织中的脂质过氧化物。

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