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作 者:赵明奇[1] 吴伟康[1] 段新芬[1] 刘颖[2] 赵丹洋[3] 梁天文[1] 罗汉川[1]
机构地区:[1]中山大学基础医学院病理生理教研室,广州510080 [2]广东药学院病理生理教研室,广州510224 [3]广州市儿童医院,广州510120
出 处:《中药材》2005年第6期486-489,共4页Journal of Chinese Medicinal Materials
摘 要:目的探讨四逆汤对阿霉素(ADR)诱导的心力衰竭大鼠心肌细胞线粒体的保护机制。方法SD大鼠随机分为对照组,心衰组和四逆汤组,心衰组和四逆汤组尾静脉注射ADR复制心衰模型,四逆汤组给予四逆汤煎剂灌胃(3.75g生药/kg/d),3周后测定大鼠心功能,线粒体丙二醛(MDA)含量,MnSOD活性,肿胀程度及Na+K+ATP酶和Ca2+ATP酶活力,RTPCR法检测MnSODmRNA表达。结果四逆汤组可以显著改善心衰大鼠心功能,提高MnSOD的活性及其mRNA表达,减少心肌细胞线粒体MDA的含量及肿胀程度,提高ATP酶活力。结论阿霉素性心力衰竭心肌细胞线粒体存在明显的氧化应激反应,四逆汤可以通过减轻氧化损伤,改善线粒体功能,保护心肌组织。Objective:The role of mitochondria in Adriamycin (ADR)-induced heart failure and the protective effects of Sini Decoction (SND) were investigated.Methods:SD rats were randomly divided into three groups,control group,heart failure group(model group) and SND group.ADR was injected in the rats of heart failure group and SND group by caudal vein.After injection,the rats in SND group were given SND (3.75/kg/d,p.o.).Three weeks later,cardiac function,mitochondrial swelling,content of malondialdehyde (MDA),activity of Mn SOD,Na+-K+ ATPase and Ca 2+ ATPase were measured.The mRNA expression of Mn SOD was also detected by RT-PCR. Results:Compared with model group,the cardiac function,the activity and the mRNA expression of Mn SOD and the activity of Na+-K+ ATPase and Ca 2+ ATPase were significantly elevated,while the degree of mitochondria swelling and the content of MDA were reduced in SND-treated rats.Conclusion:The data suggests that oxidative stress is present in the mitochondria of myocardium in ADR-induced heart failure rats and it can be reduced by SND.The mechanism may be closely related to the protective effects on mitochondria.
关 键 词:线粒体功能 大鼠心肌 阿霉素性 四逆汤 丙二醛(MDA) ATP酶活力 mRNA表达 细胞线粒体 PCR法检测 氧化应激反应 心力衰竭 尾静脉注射 SOD活性 Ca^2+ 保护机制 SD大鼠 心衰模型 氧化损伤 心肌组织 心功能 对照组 ADR Mn RT-
分 类 号:R136.31[医药卫生—劳动卫生] R541.4[医药卫生—公共卫生与预防医学]
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