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作 者:刘丹[1] 孙品兰[1] 罗明军[1] 黄春[1] 张乐星[1] 谭祥惠[1]
机构地区:[1]重庆三峡医药高等专科学校,重庆万州404120
出 处:《重庆医学》2012年第5期461-462,465,共3页Chongqing medicine
基 金:重庆市教委科学技术研究项目(KJ092101)
摘 要:目的探讨葡萄糖酸锌(ZG)对心肌缺血/再灌注损伤保护作用及其机制。方法将50只雄性SD大鼠随机分为5组,即假手术组,模型组,ZG低、中、高剂量组。采用结扎冠状动脉左前降支,引起心肌缺血,放松丝线给予再灌注的方法建立心肌缺血/再灌注损伤模型。ZG低、中、高剂量组,于末次灌胃1h后行缺血30min,再灌注60min。于再灌注结束后取心肌组织测定钠-钾-三磷酸腺苷酶(Na+-K+-ATPase)、超氧化物歧化酶(SOD)活性、IL-1β、Ca2+和丙二醛(MDA)含量。结果与模型组相比,ZG 3个剂量组大鼠心肌组织中Na+-K+-ATPase和SOD活性升高,IL-1β、Ca2+和MDA含量降低,差异有统计学意义(P<0.05)。结论 ZG对缺血/再灌注心肌具有保护作用。可能与减轻脂质过氧化反应、改善心肌能量代谢、减轻钙超载及抑制炎症反应有关。Objective To investigate the protective effect of zinc gluconate on myocardial ischemia/reperfusion injury in rats and its possible mechanism.Methods Fifty SD rats were randomly divided into five groups:sham,model,ZG of low,middle and high dose groups.Left coronary artery braid,silk suture tense and silk suture slacken were adopted to establish the model of myocardial ischemia/reperfusion injury in anesthetized rats.At 1 h after the last administration,the rats of ZG three groups were ligated for 30 min and reperfused for 60 min in the left anterior descending branch of coronary artery.Myocardial tissue was collected at the end of reperfusion for detecting the activitise of Na+-K+-ATPase and SOD,the contents of IL-1β,Ca2+ and MDA.Results Compared with the model group,the three different dose groups of ZG increased the activitise of Na+-K+-ATPase and SOD,decreased the contents of IL-1β,Ca2+ and MDA.Conclusion ZG has protective effects on myocardial ischemia/reperfusion injury.The mechanism is the inhibition of hydroxyl radical(·OH) generation,the reduction of lipid peroxidation,the improvement of cardiac energy metabolism,the reduction of calcium overload and the inhibition of inflammatory response.
关 键 词:再灌注损伤 葡萄糖酸锌 钠-钾-ATP酶 白细胞介素1Β
分 类 号:R542.22[医药卫生—心血管疾病]
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