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福辛普利对培养心肌细胞缺氧复氧性损伤的干预研究 被引量:2

The effects of Fosinopril on culture cardiocytes in hypoxia-reoxygenation injury
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摘要 目的 研究缺氧复氧性损伤的发生机制及福辛普利对损伤的影响。  方法 Wistar大鼠 5 0只 ,取其心肌细胞和主动脉内皮细胞培养 ,分离其外周血中性粒细胞 ,分设缺氧复氧正常条件培养组 (正常组 ) ,单纯缺氧复氧组 (HR组 ) ,正常培养 +白介素 1β(IL 1β ,10 0U·ml-1)刺激组 (IL 1β组 ) ,将以上 3组再分别分为 :不干预组和福辛普利干预组。于缺氧 1h后复氧 6h ,测定心肌细胞IL 1β、细胞间粘附分子 1(ICAM 1)蛋白质表达水平 ,细胞胞浆游离钙 ([Ca2 + ]i) ,一氧化氮合酶 (NOS) ,超氧化物歧化酶 (SOD) ,丙二醛 (MDA) ,还原型谷胱苷肽 (GSH)和中性粒细胞与内皮细胞粘附率。  结果 心肌细胞缺氧复氧及IL 1β刺激时 ,IL 1β、ICAM 1蛋白质表达 ,中性粒细胞与内皮细胞的粘附率、[Ca2 + ]i和MDA均有显著增加 ,而SOD、GSH、NOS明显下降 ;缺氧复氧组上述各项指标除GSH外改变较IL 1干预刺激组更显著。福辛普利可明显改善 2组MDA、中性粒细胞与内皮细胞的粘附率的增加以及SOD、GSH、NOS的下降程度 ,但对IL 1β、ICAM 1的表达水平和 [Ca2 + ]i超载增高的程度无影响。  结论  IL 1β通过直接或间接作用于ICAM 1、氧自由基和NO NOS系统引起细胞损伤 ,福辛普利可通过直接或间接调节氧自由基和NO NOS系统而减轻缺? Objective To investigate the mechanisms of hypoxia reoxygenation(HR) and the effects of Fosinopril on the cardiocytes. Methods Cardiocytes and aortic endotheliacytes from 50 rats were divided into three groups:HR group,IL 1β group and control group.Then,cells in each group were divided equally into interventions of Fosinopril and non intervention groups.Samples were observed at the time of 1 h after hypoxia and 6 h after reoxygenation.The expression of IL 1β and intercellular adhesion molecule 1 monoclona 1(ICAM 1) protein level were measured by ELISA.The adhesion rate of polymorphonuclear leukocytes(PMNs) on to endothelial cells(ECs),the content of malondialdehyde (MDA),superoxide dismutase(SOD),reduced glutathione(GSH),nitric oxide synthase(NOS),[Ca 2+ ]i,were also measured. Results The expression of ICAM 1,IL 1β protein,[Ca 2+ ]i,MDA and adhesion rate of PMNs ECs were increased and SOD,GSH,NOS were decreased at 6 h after HR.In IL 1β group,similar changes were observed.The changes of MDA,SOD,GSH,NOS and adhesion rate of PMNs ECs were attenuated by Fosinopril( P <0 05~0 01),but the expression of ICAM 1,IL 1β protein and [Ca 2+ ]i were not reduced in Fosinopril group. Conclusions The HR injury of cardiocytes can be enhanced by IL 1β through inducing the changes of SOD,GSH,NOS,[Ca 2+ ]i,expression of ICAM 1,and adhesion rate of PMNs Ecs.This injury can be partly attenuated by Fosinopril.
出处 《实用老年医学》 CAS 2003年第6期300-302,305,共4页 Practical Geriatrics
关键词 缺氧复氧性损伤 发生机制 心肌细胞 福辛普利 大鼠 氧自由基 NO-NOS系统 Hypoxia reoxygenation injury Myocardial cells Fosinopril Rats
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