Di-(2-ethylhexyl) phthalate accelerates atherosclerosis in apolipoprotein E-deficient mice

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• 作者：Jin-Feng Zhao ; Sheng-Huang Hsiao ; Ming-Hua Hsu ; Kuan-Chuan Pao…
• 关键词：DEHP ; Atherosclerosis ; Cholesterol metabolism ; Inflammation ; Obesity
• 刊名：Archives of Toxicology
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：90
• 期：1
• 页码：181-190
• 全文大小：2,949 KB
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• 作者单位：Jin-Feng Zhao (1)
  Sheng-Huang Hsiao (2)
  Ming-Hua Hsu (3)
  Kuan-Chuan Pao (3)
  Yu Ru Kou (1)
  Song-Kun Shyue (4)
  Tzong-Shyuan Lee (1)
  
  1. Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan
  2. Department of Surgery, Ren-Ai Taipei City Hospital, Taipei, 10629, Taiwan
  3. Nuclear Science and Technology Development Center, National Tsing Hua University, Hsinchu, 30013, Taiwan
  4. Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan
  
• 刊物主题：Pharmacology/Toxicology; Occupational Medicine/Industrial Medicine; Environmental Health; Biomedicine general;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-0738

文摘

Di-(2-ethylhexyl) phthalate (DEHP) is associated with atherosclerosis-related cardiovascular disease complications, but we lack direct evidence of its unfavorable effect on atherogenesis. In this study, we aimed to clarify in vivo and in vitro the contribution of DEHP to the development of atherosclerosis and its underlying mechanisms. Apolipoprotein E-deficient (apoE−/−) mice chronically treated with DEHP for 4 weeks showed exacerbated hyperlipidemia, systemic inflammation, and atherosclerosis. In addition, DEHP promoted low-density lipoprotein (LDL) oxidation, which led to inflammation in endothelial cells as evidenced by increased protein expression of pro-inflammatory mediators. Furthermore, chronic DEHP treatment increased hepatic cholesterol accumulation by downregulating the protein expression of key regulators in cholesterol clearance including LDL receptor, cholesterol 7α-hydrolase, ATP-binding cassette transporter G5 and G8, and liver X receptor α. Moreover, the adiposity and inflammation of white adipose tissues were promoted in DEHP-treated apoE−/− mice. In conclusion, DEHP may disturb cholesterol homeostasis and deregulate the inflammatory response, thus leading to accelerated atherosclerosis.