Intermedin inhibits uptake of oxidized LDL via CD36 pathway in RAW264.7 cells

被引：1

作者：

Wang, Yong ^{[1
]}

Yang, Rui ^{[1
]}

Chen, Xiaoni ^{[1
]}

Zhang, Xin ^{[1
]}

He, Sen ^{[1
]}

Feng, Jiayue ^{[1
]}

Wan, Shixi ^{[1
]}

Wang, Si ^{[1
]}

Chen, Xiaoping ^{[1
]}

机构：

[1] Sichuan Univ, West China Hosp, Dept Cardiovasc Med, Chengdu 610041, Peoples R China

来源：

PHARMAZIE | 2014年 / 69卷 / 06期

基金：

中国国家自然科学基金;

关键词：

SCAVENGER RECEPTOR; PPAR-GAMMA; ATHEROSCLEROSIS; MICE; MACROPHAGES; IDENTIFICATION;

D O I：

10.1691/ph.2014.3941

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

Intermedin (IMD) exerts a potent function in preventing atherosclerosis, while the mechanism remains unclear. Here we investigated the potential molecular mechanism responsible for the protective function of IMD in preventing foam cell formation in RAW264.7 cells. In our present study, IMD significantly inhibited intracellular cholesterol accumulation. Additionally, IMD dose-dependently down-regulated CD36 expression, which was confirmed by real-time quantitative reverse transcription-PCR and Western blot analysis. Our data suggest that IMD could inhibit the formation of foam cells through, at least partly, a CD36-dependent mechanism. This study suggests that IMD may be a therapeutic candidate for treating atherosclerosis.

引用

页码：473 / 476

页数：4

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