实验性脑缺血再灌注时超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性的变化。

S Işlekel, H Işlekel, G Güner, N Ozdamar
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引用次数: 74

摘要

自由基被认为是缺血后再灌注损伤的最重要原因。缺血再灌注后组织的抗氧化状态对机体对自由基损伤的初级内源性防御具有重要意义。本实验采用大鼠脑全脑中度(半暗)缺血模型,对缺血-再灌注期脑组织抗氧化酶能力进行了评价。实验在45只雄性斯普拉格大鼠身上进行。双侧椎动脉烧灼和双侧颈动脉临时闭塞诱导缺血,持续10分钟。在缺血结束(0 min再灌注)和不同再灌注时间(20 min、60 min、240 min),取大鼠头颅,液氮冷冻脑。用分光光度法测定大鼠脑组织细胞内抗氧化酶(超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶)活性的变化。与假手术对照组相比,所有中度缺血再灌注组的超氧化物歧化酶活性均显著降低(P < 0.05)。缺血时,超氧化物歧化酶活性降至对照组的31%。再灌注组下降更明显,特别是在60分钟再灌注时(40%)。谷胱甘肽过氧化物酶活性降低幅度较小,但仍显著(P < 0.05)。再灌注20 min和60 min时,大鼠脑缺血程度明显下降,占26%。相反,中度缺血再灌注使过氧化氢酶活性显著升高(P < 0.05)。中度缺血10 min时,其增加量为缺血前水平的63%。由此可见,中度脑缺血再灌注时,主要抗氧化酶活性发生了显著变化。这些结果表明,氧化-抗氧化平衡的紊乱可能在使组织更容易受到自由基诱导的损伤中起作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Alterations in superoxide dismutase, glutathione peroxidase and catalase activities in experimental cerebral ischemia-reperfusion.

Free radicals are thought to be the most important cause of the reperfusion injury subsequent to ischemia. The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free radical induced injury. This investigation was performed to evaluate the antioxidant enzyme capacity of the brain tissue in the ischemia-reperfusion period using an experimental global moderate (penumbral) ischemia model on rat brains. Experiments were performed on 45 male Sprague Dawley rats. Ischemia was induced by bilateral vertebral arteries cauterization and temporary bilateral carotid arteries occlusion and sustained for 10 minutes. At the end of ischemia (0 min reperfusion) and various reperfusion periods (20 min, 60 min, 240 min), rats were decapitated and brains were frozen in liquid nitrogen. Changes in the intracellular antioxidant enzyme (superoxide dismutase, glutathione peroxidase and catalase) activities were assessed in the rat brain tissues, by spectrophotometric methods. In all moderate ischemia-reperfusion groups, superoxide dismutase activities were found to have decreased significantly compared to the sham operated controls (P < 0.05). During ischemia superoxide dismutase activity was lowered to 31% of that of the control group. The decreases were more significant in reperfusion groups, particularly in 60 min reperfusion (40%). Relatively smaller but still significant diminution was observed in glutathione peroxidase activities (P < 0.05). The ratio of diminution was striking in 20 min and 60 min reperfusion groups with 26% of the sham operated rats. Conversely, moderate ischemia-reperfusion caused significant increase in catalase activities (P < 0.05). The increment was 63% of the preischemic level with 10 min of moderate ischemia. In conclusion, activities of the major antioxidant enzymes were changed significantly in moderate brain ischemia-reperfusion. These results suggest that the disturbance in oxidant-antioxidant balance might play a part in rendering the tissue more vulnerable to free radical induced injuries.

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