邻苯二甲酸二（2-乙基己基）酯加重大鼠非酒精性脂肪肝病及其潜在机制。
Di(2-ethylhexyl) phthalate exacerbates non-alcoholic fatty liver in rats and its potential mechanisms.
机构信息
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.
Affiliated Anhui Provincial Hospital, Anhui Medical University, Hefei 230001, Anhui, China.
出版信息
Environ Toxicol Pharmacol. 2016 Mar;42:38-44. doi: 10.1016/j.etap.2015.12.016. Epub 2015 Dec 25.
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.
邻苯二甲酸二（2-乙基己基）酯（DEHP）可能导致类似于非酒精性脂肪性肝病（NAFLD）的变化。本研究的目的是通过直接触发肝脏脂质代谢紊乱或间接通过肝毒性作用来研究 DEHP 对脂肪肝大鼠的有害影响和可能的机制。考虑到这些影响，DEHP 可能在 NAFLD 的发病机制中起重要作用。在这项研究中，高脂饮食用于诱导大鼠非酒精性脂肪性肝病 8 周。在整个实验期间，DEHP 处理组通过灌胃分别给予（0.05、5、500mg/kg/天）剂量。我们的结果表明，DEHP 对高脂饮食诱导的 NAFLD 的有害影响是通过增加肝脏中的脂质积累、引起脂质过氧化和炎症来介导的。
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