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实验性肾病中低密度脂蛋白的大小及氧化易感性

LDL size and susceptibility to oxidation in experimental nephrosis.

作者信息

Posadas-Sánchez R, Posadas-Romero C, Zamora-González J, Hernández-Ono A, Baños-Marhaber G, Campos O N, Pedraza-Chaverrí J

机构信息

Departamento de Endocrinología del Instituto Nacional de Cardiología Ignacio Chavez, Mexico City, Mexico.

出版信息

Mol Cell Biochem. 2001 Apr;220(1-2):61-8. doi: 10.1023/a:1010874306937.

Abstract

The aim of this study was to investigate the relationship between endothelial dysfunction and low density lipoprotein (LDL) size and susceptibility to oxidation in nephrotic rats with or without deficiency of vitamin E and selenium. Four groups of male Wistar rats were studied: control (C), vitamin E and selenium deficient control (DefC), nephrotic (NS), and vitamin E and selenium deficient NS (DefNS). Nephrotic syndrome was induced by puromycin aminonucleoside. The molar ratio of vitamin E/LDL-cholesterol was significantly lower in DefNS, DefC rats, and NS vs. C rats. In comparison with control animals, vasodilation and LDL oxidability were significantly lower in nephrotic animals. LDL size was similar in all groups. Abnormal endothelial function in response to acetylcholine and carbachol was observed in NS animals compared to control rats. Relaxation response was inversely associated with an increase in LDL susceptibility to oxidation and with a lower molar ratio of vitamin E/LDL-c. LDL oxidability and LDL-c were the only variables independently associated with vasodilation. These results suggest that endothelial dysfunction of NS may be a consequence of the increased LDL susceptibility to oxidation, secondary to antioxidant deficiency.

摘要

本研究旨在调查在有或没有维生素E和硒缺乏的肾病大鼠中,内皮功能障碍与低密度脂蛋白(LDL)大小及氧化易感性之间的关系。研究了四组雄性Wistar大鼠:对照组(C)、维生素E和硒缺乏对照组(DefC)、肾病组(NS)以及维生素E和硒缺乏肾病组(DefNS)。通过嘌呤霉素氨基核苷诱导肾病综合征。与C组大鼠相比,DefNS组、DefC组大鼠以及NS组大鼠中维生素E/LDL-胆固醇的摩尔比显著降低。与对照动物相比,肾病动物的血管舒张和LDL氧化能力显著降低。所有组的LDL大小相似。与对照大鼠相比,NS组动物对乙酰胆碱和卡巴胆碱的反应出现内皮功能异常。舒张反应与LDL氧化易感性增加以及维生素E/LDL-c摩尔比降低呈负相关。LDL氧化能力和LDL-c是与血管舒张独立相关的仅有的变量。这些结果表明,肾病的内皮功能障碍可能是抗氧化剂缺乏继发的LDL氧化易感性增加的结果。

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