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Environ Toxicol Pharmacol. 2016 Mar;42:38-44. doi: 10.1016/j.etap.2015.12.016. Epub 2015 Dec 25.

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

Author information

1
Institute of Clinical Pharmacology of Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, Anhui, China.
2
Affiliated Anhui Provincial Hospital, Anhui Medical University, Hefei 230001, Anhui, China. Electronic address: xu_weiping666@163.com.
3
Institute of Clinical Pharmacology of Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, Anhui, China. Electronic address: wwei@ahmu.edu.cn.

Abstract

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.

KEYWORDS:

DEHP; Inflammation; Lipid accumulation; NAFLD

PMID:
26773359
DOI:
10.1016/j.etap.2015.12.016
[Indexed for MEDLINE]

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