脑缺血大鼠促氧化-抗氧化平衡紊乱

E. Bon', N. E. Maksimovich, I. Dremza, M. A. Nosovich, K. A. Khrapovitskaya
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引用次数: 2

摘要

活性氧过量可导致膜损伤,脂质、蛋白质和核酸氧化产物的积累,线粒体膜的还原吡啶核苷酸和磷脂缺乏,进而导致电解质失衡,线粒体肿胀,氧化和磷酸化过程解耦,缺血性神经元死亡。因此,对氧化应激和抗氧化系统活性的研究具有重要意义。本研究旨在探讨不同严重程度缺血性脑损伤大鼠(次全脑缺血和全脑缺血)中促氧化-抗氧化平衡的变化。材料与方法。根据欧洲议会和欧盟理事会2010年9月22日第2010/63/EU号关于科学用动物保护的指令要求,实验对象为30只体重为260±20 g的雄性近交大鼠。结果。蛋白质和谷胱甘肽的总sh -基团含量显著降低(减少58 (51;64) % (p<0.05), GSH浓度为29 (19;与1小时脑缺血相比,24小时次全脑缺血(SBI)组的死亡率为35% (p<0.05)。谷胱甘肽过氧化物酶活性的变化是多向的:在1小时SBI中,活性增加了12 (9);18) % (p<0.05), 24小时SBI降低74 (67;81) % (p<0.05)。在SBI 1小时内,蛋白质和谷胱甘肽的总sh基团含量增加了60 (54;65) % (p<0.05), GSH浓度高42 (39;与1小时全脑缺血(TBI)相比,p<0.05。与硫代巴比妥酸反应的产物含量增加了59 (51;63) % (p<0.05)。在24小时的SBI中,蛋白质和谷胱甘肽的总sh基团含量增加了36 (29;45) % (p<0.05), GSH浓度比对照组高63 (59;75) % (p<0.05)。与硫代巴比妥酸反应的产物含量增加了83 (78;91) % (p<0.05)。脑外伤后谷胱甘肽过氧化物酶活性为零。结论。因此,在24小时TBI中观察到促氧化-抗氧化平衡最明显的紊乱。在24小时SBI中观察到类似但不太明显的干扰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DISTURBANCE OF PRO-OXIDANT-ANTIOXIDANT BALANCE IN RATS WITH CEREBRAL ISCHEMIA
Excess of reactive oxygen can lead to membrane damage, accumulation of lipid, protein, and nucleic acid oxidation products, deficiency of reduced pyridine nucleotides and phospholipids of mitochondrial membranes, and then to electrolyte imbalance, mitochondrial swelling, uncoupling of oxidation and phosphorylation processes, and ischemic neuronal death. Thus, the study of oxidative stress and antioxidant system activity is relevant. The aim of the study is to examine the changes in the pro-oxidant-antioxidant balance in rats with ischemic brain damage of different degrees of severity (subtotal and total cerebral ischemia). Materials and Methods. The experiments were performed on 30 male outbred white rats weighing 260±20 g in compliance with the requirements of the Directive of the European Parliament and the Council of the European Union No. 2010/63/EU of September 22, 2010 on the protection of animals used for scientific purposes. Results. A more significant decrease in the content of total SH-groups of proteins and glutathione (by 58 (51; 64) % (p<0.05)), and GSH concentration (by 29 (19; 35) % (p<0.05)) was observed under 24-hour subtotal brain ischemia (SBI) compared with 1-hour SBI. Changes in the glutathione peroxidase activity were multidirectional: in 1-hour SBI, the activity increased by 12 (9; 18) % (p<0.05compared to the control level, and in 24-hour SBI, it decreased by 74 (67; 81) % (p<0.05). In 1-hour SBI, the content of total SH-groups of proteins and glutathione was higher by 60 (54; 65) % (p<0.05), and GSH concentration was higher by 42 (39; 56) % (p<0.05) compared with 1-hour total brain ischemia (TBI). The content of products that react with thiobarbituric acid increased by 59 (51; 63) % (p<0.05). In 24-hout SBI, the content of total SH-groups of proteins and glutathione was higher by 36 (29; 45) % (p<0.05), and GSH concentration was higher by 63 (59; 75) % (p<0.05) compared with 24-hour TBI. The content of products that react with thiobarbituric acid increased by 83 (78; 91) % (p<0.05). The glutathione peroxidase activity in TBI was equal to zero. Conclusions. Thus, the most pronounced disturbances in the pro-oxidant-antioxidant balance were observed in 24-hour TBI. Similar, but less pronounced disturbances were observed in 24-hour SBI.
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