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作 者:张小丽
机构地区:[1]浙江省长兴县人民医院药剂科,浙江长兴313100
出 处:《药学进展》2010年第1期30-35,共6页Progress in Pharmaceutical Sciences
摘 要:目的:探讨大蒜素对阿霉素性心衰大鼠心功能的保护作用及其线粒体机制。方法:将雄性SD大鼠随机分为正常对照组、大蒜素对照组、心衰模型组和不同剂量的大蒜素治疗组。给心衰模型组和大蒜素治疗组大鼠尾静脉注射阿霉素(4mg.kg-1,每5天1次,共3次),第3次注射后,给大蒜素治疗组大鼠经口使用大蒜素(剂量分别为3、10和30mg.kg-1.d-1),3周后测定该组大鼠左心室血流动力学指标、线粒体活性氧(ROS)和丙二醛(MDA)含量、线粒体肿胀程度以及线粒体超氧化物歧化酶(SOD)、Na+-K+-ATP酶和Ca2+-ATP酶的活性。结果:治疗3周后,与心衰模型组相比,大蒜素治疗组大鼠左心室发展压、左心室内压最大上升和下降速率显著提高,左心室舒张末压力升高的状况明显减轻,心肌线粒体ROS、MDA含量明显降低,线粒体肿胀程度显著降低,线粒体SOD活性和ATP酶活性明显提高,且上述变化均呈剂量依赖性。结论:大蒜素可剂量依赖性减轻阿霉素性心衰大鼠的心功能损伤,这种保护作用可能与其提高线粒体抗氧化能力、减轻氧化应激损伤、抑制线粒体肿胀及维持膜ATP酶活性有关。] Objective: To explore the effects of allicin on reducing cardiac dysfunction in rats with adriamycin (ADR)-induced heart failure and the related mitoehondrial mechanism. Methods: Male SD rats were randomly divided into normal control group, alliein control group, heart failure model group and allicin treatment groups at different doses. The rats of heart failure model group and allicin treatment groups were given ADR (4 mg.kg-1) by tail vein once every five days, three times totally. Then after the third injection, the allicin treatment groups of low, medium and high dose were given allicin ( 3, 10 and 30 mg.kg-1.d-1, respectively) by intragastrie perfusion for three weeks. The left ventricular hemodynamie parameters, the level of reactive oxygen species (ROS) and malondialdehyde (MDA) in cardiac mitochon- dria, the degree of mitochondrial swelling, and the activities of superoxide dismutase (SOD), Na + -K + - ATPase and Ca2+ -ATPase were measured after the treatment. Results: Compared with heart failure model group, the left ventricular developed pressure and maximal rise/fall rate of left ventricular pressure were markedly enhanced, and left ventricular end diastolic pressure was decreased in allicin treatment groups. Moreover, the level of cardiac mitochondrial ROS and MDA, and the degree of mitochondrial swelling were markedly decreased, while the activities of mitochondrial SOD, Na + -K+ -ATPase and Ca2+ -ATPase were significantly elevated in allicin treatment groups. The above changes of the parameters were all dose- dependent. Conclusion: The treatment with allicin can reduce cardiac dysfunction in rats with ADR-induced heart failure. All the effect may be related with enhancing mitochondrial anti-oxidative ability, decreasing oxidative stress injury and the degree of mitochondrial swelling, and maintaining mitochondrial ATPase activity.
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