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大鼠短暂性前脑缺血后脑脊液和海马中内源性抗氧化酶的活性

Activities of endogenous antioxidant enzymes in the cerebrospinal fluid and the hippocampus after transient forebrain ischemia in rat.

作者信息

Danielisová Viera, Gottlieb Miroslav, Némethová Miroslava, Burda Jozef

机构信息

Institute of Neurobiology, Slovak Academy of Sciences, Soltesovej 6, 040 01 Kosice, Slovak Republic.

出版信息

J Neurol Sci. 2007 Feb 15;253(1-2):61-5. doi: 10.1016/j.jns.2006.12.001. Epub 2007 Jan 9.

DOI:10.1016/j.jns.2006.12.001
PMID:17215005
Abstract

The activity of SOD and CAT was measured in controls and 5 h after 5, 10 and 15 min of ischemia, as well as 1 or 2 days after 10 min of ischemia in the hippocampus and in the CSF. A significant increase in total SOD activity 5 h after ischemia was caused mainly by increased CuZn-SOD activity. The highest values were measured 5 h after 5 min ischemia (by 160%) and smallest if 15 min (by 40%) of ischemia was used. In comparison to the hippocampus, the activity of SOD in CSF increased equally after all intervals of ischemia. Activities of total SOD and CuZn-SOD after 10 min of ischemia in the hippocampus were significantly increased only after 5 and 24 h of reperfusion but in CSF they were increased after all examined intervals of reperfusion. The activity of CAT was significantly increased in the hippocampus after 5 (by 260%), 10 and 15 min (by 100%) of ischemia. CAT activity in CSF was increased equally after all intervals of ischemia (by 200%). Ischemic attack causes a rapid response in hippocampal tissue as well as in the CSF, represented by an increase in the activity of endogenous antioxidant enzymes SOD and CAT.

摘要

在对照组以及海马体和脑脊液中,分别于缺血5、10和15分钟后的5小时,以及缺血10分钟后的1天或2天测量超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。缺血后5小时总SOD活性显著增加,主要是由于铜锌超氧化物歧化酶(CuZn-SOD)活性增加所致。缺血5分钟后5小时测得的值最高(增加160%),而使用缺血15分钟时测得的值最小(增加40%)。与海马体相比,脑脊液中SOD的活性在所有缺血间隔后均同等增加。海马体缺血10分钟后,总SOD和CuZn-SOD的活性仅在再灌注5小时和24小时后显著增加,但在脑脊液中,它们在所有检查的再灌注间隔后均增加。缺血5分钟(增加260%)、10分钟和15分钟(增加100%)后,海马体中CAT的活性显著增加。脑脊液中CAT的活性在所有缺血间隔后均同等增加(增加200%)。缺血发作会导致海马组织以及脑脊液中出现快速反应,表现为内源性抗氧化酶SOD和CAT的活性增加。

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