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作 者:黄琳[1] 陆付耳[1] 杨小玉[1] 陆小红 陈广[1] 闫忠卿[1] 汪智全[1]
机构地区:[1]华中科技大学同济医学院附属同济医院中西医结合研究所,武汉430030 [2]湖北天茂集团制剂厂
出 处:《中国中西医结合杂志》2008年第8期725-728,共4页Chinese Journal of Integrated Traditional and Western Medicine
基 金:国家自然科学基金资助项目(No.30500685)
摘 要:目的研究黄连解毒汤对胰岛素抵抗大鼠氧自由基所致肝脏线粒体损伤的保护作用,并探讨其作用机制。方法高脂饲料喂养Wistar大鼠,建立胰岛素抵抗模型;造模成功后随机分为黄连解毒汤组、小檗碱组、硫辛酸组和模型组,各组以相应的药物干预6周;测定肝脏线粒体ATP酶、琥珀酸脱氢酶(SDH)、细胞色素C氧化酶(CCO)活性及ATP含量以观察线粒体功能及能量代谢活性;测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量以观察线粒体抗氧化能力。结果黄连解毒汤能提高胰岛素抵抗大鼠肝脏线粒体中GSH-Px、SOD、ATP酶活力,抑制MDA生成,促进能量生成代谢,增强SDH和CCO活力。结论黄连解毒汤可以改善线粒体功能及能量代谢,增强线粒体抗氧化能力,对胰岛素抵抗大鼠肝脏线粒体损伤有明显保护作用,其机制可能与清除氧自由基、抑制脂质过氧化有关。Objective To study the protective effects of Huanglian Jiedu Decoction (HLJD) on the oxidative damage of liver mitochondria in insulin resistant rats and to explore its possible mechanism. Methods Male Wistar rats were fed with high-fat diet to set up an insulin resistant model, and randomly divided into four groups, the con- trol group and three test groups intervened respectively with HLJD, berberine, and thioctic acid for 6 weeks. The liver mitochondrial function and energy metabolic capability were assayed by measuring the activities of ATPase, succinic dehydrogenase (SDH), cytochrome oxidase (CCO) and the content of ATP in liver tissue. The anti-oxi- dation capability of liver mitochondria was determined by measuring the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA). Results HLJD showed the effect in improving the activities of GSH-Px, SOD and ATPase, inhibiting the production of MDA, promoting the energy metabolism and strengthening the activities of SDH and CCO in liver tissue of insulin resistant rats. Conclu- sion HLJD could improve the liver mitochondria function and energy metabolism, strengthen the mitochondrial an- ti-oxidation capacity, and showed evidently protective effect on liver mitochondrial damage in insulin resistant rats. The mechanism might be correlated with its scavenging action on oxygen radicals and inhibition on lipid-peroxidation.
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