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阿托伐他汀增强高胆固醇血症兔脂肪细胞对氧化型低密度脂蛋白的摄取。

Atorvastatin enhances cellular uptake of oxidized LDL in adipocytes from hypercholesterolemic rabbits.

作者信息

Zhao Shui-Ping, Zhang Da-Qing

机构信息

Department of Cardiology, The Second XiangYa Hospital of Central South University, 410011, Changsha, PR China

出版信息

Clin Chim Acta. 2004 Jan;339(1-2):189-94. doi: 10.1016/j.cccn.2003.10.007.

Abstract

BACKGROUND

Peroxisome proliferator-activated receptor gamma (PPARgamma) and CD36, a plausible pathway for the oxidized low-density lipoprotein (ox-LDL) uptake in monocytes, is highly expressed in adipocytes. Few studies have explored the cellular uptake of ox-LDL in adipocytes and its significance on atherosclerosis.

METHODS

Rabbits on high-cholesterol diets were randomly assigned to either 1.5 mg/kg/day atorvastatin (n = 5) or starch (n = 5) for 2 weeks. Subcutaneous adipose tissues were collected for adipocytes culture. The uptake of 125I-OxLDL in adipocytes was determined by a gamma-counter and each sample was normalized to protein concentration. Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate PPARgamma and CD36 mRNA expressions.

RESULTS

Adipocytes took up 125I-OxLDL in a concentration-dependent manner. Two weeks of atorvastatin treatment enhanced the cellular uptake of 125I-OxLDL, which was closely related to the reduced plasma low-density lipoprotein cholesterol (LDL-C) concentrations and increased mRNA expressions of PPARgamma and CD36 in adipocytes, respectively.

CONCLUSIONS

Adipocytes may be a potential pool for plasma ox-LDL, and atorvastatin can improve the ox-LDL uptake in adipocytes possibly through reducing cholesterol concentration and upregulating mRNA expressions of PPARgamma and CD36.

摘要

背景

过氧化物酶体增殖物激活受体γ(PPARγ)和CD36是单核细胞摄取氧化型低密度脂蛋白(ox-LDL)的一条可能途径,在脂肪细胞中高表达。很少有研究探讨脂肪细胞对ox-LDL的摄取及其在动脉粥样硬化中的意义。

方法

将高胆固醇饮食的兔子随机分为两组,分别给予1.5mg/kg/天的阿托伐他汀(n = 5)或淀粉(n = 5),持续2周。收集皮下脂肪组织用于脂肪细胞培养。用γ计数器测定脂肪细胞对125I-OxLDL的摄取,并将每个样品标准化为蛋白质浓度。采用逆转录聚合酶链反应(RT-PCR)评估PPARγ和CD36 mRNA的表达。

结果

脂肪细胞以浓度依赖的方式摄取125I-OxLDL。阿托伐他汀治疗2周增强了脂肪细胞对125I-OxLDL的摄取,这分别与血浆低密度脂蛋白胆固醇(LDL-C)浓度降低以及脂肪细胞中PPARγ和CD36 mRNA表达增加密切相关。

结论

脂肪细胞可能是血浆ox-LDL的一个潜在储存库,阿托伐他汀可能通过降低胆固醇浓度和上调PPARγ和CD36的mRNA表达来改善脂肪细胞对ox-LDL的摄取。

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