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机构地区:[1]中国医学科学院中国协和医科大学基础医学研究所生理研究室,北京100005
出 处:《基础医学与临床》2005年第9期838-841,共4页Basic and Clinical Medicine
摘 要:目的探讨活性氧在心肌细胞低氧预适应过程中的作用机制。方法建立SD乳鼠心肌细胞的低氧预适应模型;检测不同阶段超氧阴离子和H2O2含量以及T-SOD、Cu,Zn-SOD和Mn-SOD活性变化,分析活性氧在低氧预适应不同窗口期的作用。结果(1)超氧阴离子和过氧化氢均能明显提高心肌细胞在第一窗口期低氧1h后的存活率(P<0·05);(2)超氧阴离子可明显升高心肌细胞第二窗口期低氧1h后的存活率(P<0·05),而过氧化氢作用不明显;(3)低氧预适应可使超氧阴离子和过氧化氢含量明显升高,同时伴有第一窗口期Cu、Zn-SOD活性及第二窗口期Mn-SOD活性显著升高(P<0·05)。结论说明低氧预适应可提高大鼠心肌细胞在不同窗口期对长时间缺氧的耐受性,其作用机制可能与活性氧及SOD有密切关系。Objective A hypoxic precongditioning model constructed by cultured cardiomyocytes of Sprague-Dawley rats was developed exposure of the animals to short-term and repeated hypoxia and reoxygenation (5 min hypoxia + 10 min reoxygenation) and thereby to exclude the effect from the peripheral sympathetic nerve, endothelial cells, neutrophils and inflammatory factors. Methods With this model, we examined the concentration of superoxide anion and H2O2 as well as the activity of SOD to find the possible pathway of preconditioning. Results Both superoxide anion and H2O2 can initiate the early phase of preconditioning. Short-term hypoxia can increased the production of superoxide anion and in sequence transitorily activate Cu, Zn-SOD, which leads to production of H2O2, an active signalng agent in this term of preconditioning. In late phase of preconditioning, the increased superoxide anion that activates Mn-SOD alleviate the injury of hypoxia. Conclusion Oxygen free radicals produced during brief, intermittent hypoxia may increases activity of different antioxidant enzymes in different terms of hypoxic preconditioning, This mechanision seem to be responsible for protecting myocytes from hypoxia injury.
关 键 词:心肌细胞 低氧预适应 窗口期 活性氧 超氧化物歧化酶
分 类 号:R541[医药卫生—心血管疾病]
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