Di(2-ethylhexyl) phthalate exacerbates non-alcoholic fatty liver in rats and its potential mechanisms

被引：77
作者：
Chen, Hao [1 ]
Zhang, Wang [1 ]
Rui, Bei-bei [1 ]
Yang, Si-min [1 ]
Xu, Wei-ping [2 ]
Wei, Wei [1 ]
机构：
[1] Anhui Med Univ, Key Lab Antiinflammatory & Immune Med, Anhui Collaborat Innovat Ctr Antiinflammatory & I, Inst Clin Pharmacol,Educ Minist, Hefei 230032, Anhui, Peoples R China
[2] Anhui Med Univ, Affiliated Anhui Prov Hosp, Hefei 230001, Anhui, Peoples R China
来源：
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2016年 / 42卷
关键词：
DEHP; NAFLD; Lipid accumulation; Inflammation; LIPID-METABOLISM; PPAR-ALPHA; PEROXISOME PROLIFERATOR; GENE-EXPRESSION; EXPOSURE; DISEASE; CELLS; DEHP; MICE; DIET;
D O I：
10.1016/j.etap.2015.12.016
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
Di(2-ethylhexyl) phthalate (DEHP) may be responsible for inducing alterations similar to those encountered in nonalcoholic fatty liver disease (NAFLD). The aim of the present study was to investigate the detrimental effects and possible mechanisms of DEHP on fatty liver rats directly through triggering the disorder of liver lipid metabolism or indirectly by hepatotoxic effect. Considering these effects, DEHP may play a significant role in the pathogenesis of NAFLD. In this study, high-fat diet was used to induce NAFLD in rats for eight weeks. DEHP treated groups received (0.05, 5, 500 mg/kg daily, respectively) dose by gavage during the whole experiment period. Our results indicated that the detrimental effects of DEHP on high-fat diet induced NAFLDs were mediated via increasing lipid accumulation in the liver and causing lipid peroxidation and inflammation. (C) 2015 Elsevier B.V. All rights reserved.
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页码：38 / 44
页数：7
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