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目的:超氧化物歧化酶是机体内广泛存在的酶家族,可有效催化超氧阴离子的歧化反应。人脑中有3种超氧化物歧化酶,在缺血损伤时均发挥了有益作用。近年来以基因工程鼠作为工具研究脑缺血时超氧化物歧化酶的保护作用。资料来源:应用计算机检索Medline数据库1991-01/2003-12期间的相关文章,检索词为“ChanPHandsuperoxidedismutaseandcerebralis-chemia”,限定文章语言种类为英文。资料选择:对资料进行初审,选取实验包括上述干预组(转基因组)和对照组的文献,筛除非随机的实验,对剩余的文献开始查找全文,以随机对照实验作为纳入标准。资料提炼:共收集到38篇关于脑缺血与超氧化物歧化酶关系的随机和非随机实验,13个实验符合纳入标准,排除的25篇实验中,15篇为重复实验,10篇与本文无相关性。资料综合:研究表明,活性氧参与了缺血中枢神经系统的氧化还原信号传导通路,并直接造成生物大分子如脂类,蛋白质,核酸的损伤。在缺血性脑损伤中,氧自由基产生过多及超氧化物歧化酶的消耗导致了组织细胞的损伤。铜锌超氧化物歧化酶,锰超氧化物歧化酶,细胞外超氧化物歧化酶的功能相同,可将超氧阴离子自由基分解成过氧化氢而进一步分解。从而改善脑水肿,缩小脑梗死灶及减少神经元死亡,改善缺血时的功能障碍。结论:氧自由基增加是脑缺血损伤的重要机制,3种超氧化物歧化酶均可改善脑缺血时的功能损伤,这种保护作用与其对核酸修复酶、转录因子、凋亡相关蛋白和信号转导通路等作用相关。
OBJECTIVE: Superoxide dismutase (SOD) is a widely existing family of enzymes that catalyze the disproportionation of superoxide anions. There are three types of superoxide dismutase in the human brain that play a beneficial role in ischemic injury. In recent years, genetic engineering mice as a tool to study the protective effect of superoxide dismutase during cerebral ischemia. DATA SOURCES: A computer-based online search of Medline database was conducted between January 1991 and December 2003 with the search term “ChanPHandsuperoxidedismutaseandcerebralis-chemia”. The limited article language is English. Data selection: The data were first reviewed. The experiments including the intervention group (transgenic group) and the control group were selected, and the non-randomized experiments were screened out. The remaining documents were searched for the full text, and randomized controlled trials were included as inclusion criteria. DATA EXTRACTION: A total of 38 randomized and nonrandomized experiments on the relationship between cerebral ischemia and superoxide dismutase were collected. Thirteen experiments met the inclusion criteria, of which 25 were excluded, 15 were duplicates, 10 were No correlation. DATA SYNTHESIS: Studies have shown that ROS participates in the redox signaling pathway of the ischemic central nervous system and directly damages biological macromolecules such as lipids, proteins and nucleic acids. In ischemic brain injury, excessive production of oxygen free radicals and depletion of superoxide dismutase cause tissue cell damage. Copper-zinc superoxide dismutase, manganese superoxide dismutase and extracellular superoxide dismutase have the same functions, and can decompose the superoxide anion radical into hydrogen peroxide and further decompose. Thereby improving cerebral edema, reduce cerebral infarction and reduce neuronal death, improve dysfunction in ischemia. CONCLUSION: The increase of oxygen free radicals is an important mechanism of cerebral ischemia injury. All three superoxide dismutase can improve the functional injury of cerebral ischemia, and its protective effect is related to its effect on nucleic acid repair enzyme, transcription factor, apoptosis related protein And signal transduction pathway and so on.