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二亚油酰磷脂酰胆碱可降低乙醇诱导的细胞色素P4502E1水平。

Dilinoleoylphosphatidylcholine decreases ethanol-induced cytochrome P4502E1.

作者信息

Aleynik M K, Lieber C S

机构信息

Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, Bronx, New York 10468, USA.

出版信息

Biochem Biophys Res Commun. 2001 Nov 9;288(4):1047-51. doi: 10.1006/bbrc.2001.5870.

DOI:10.1006/bbrc.2001.5870
PMID:11689017
Abstract

Cytochrome P4502E1 (CYP2E1) induction by ethanol contributes to alcoholic liver disease and we found that a mixture of polyunsaturated phosphatidylcholines (PPC), which protects against alcohol-induced liver injury, also decreases CYP2E1. Since dilinoleoylphosphatidylcholine (DLPC) is the major component of PPC, we assessed here whether it is responsible for the protection of PPC by feeding rats for 8 weeks our liquid diet containing ethanol (36% of energy) or isocaloric carbohydrates, with either DLPC (1.5 g/1000 cal), PPC (3 g/1000 cal), or linoleate. CYP2E1 was assessed by Western blots and by two of its enzyme activities: the microsomal ethanol-oxidizing system (MEOS) and p-nitrophenolhydroxylase (PNP). With ethanol, CYP2E1 increased 10-fold, with corresponding rises in PNP and MEOS activities. Compared to linoleate, DLPC significantly decreased cytochrome b(5), total cytochromes P450, CYP2E1 content and its corresponding activities. DLPC decreases ethanol-induced CYP2E1 and should be considered for the prevention of alcoholic liver disease.

摘要

乙醇诱导细胞色素P4502E1(CYP2E1)会导致酒精性肝病,我们发现,具有预防酒精性肝损伤作用的多不饱和磷脂酰胆碱(PPC)混合物也能降低CYP2E1水平。由于二亚油酰磷脂酰胆碱(DLPC)是PPC的主要成分,我们在此评估它是否是PPC发挥保护作用的原因:用含乙醇(占能量的36%)或等热量碳水化合物的流质饮食喂养大鼠8周,饮食中分别添加DLPC(1.5 g/1000卡路里)、PPC(3 g/1000卡路里)或亚油酸酯。通过蛋白质免疫印迹法以及CYP2E1的两种酶活性:微粒体乙醇氧化系统(MEOS)和对硝基苯酚羟化酶(PNP)来评估CYP2E1。给予乙醇时,CYP2E1增加了10倍,PNP和MEOS活性相应升高。与亚油酸酯相比,DLPC显著降低了细胞色素b(5)、细胞色素P450总量、CYP2E1含量及其相应活性。DLPC可降低乙醇诱导的CYP2E1,应考虑将其用于预防酒精性肝病。

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Dilinoleoylphosphatidylcholine decreases ethanol-induced cytochrome P4502E1.二亚油酰磷脂酰胆碱可降低乙醇诱导的细胞色素P4502E1水平。
Biochem Biophys Res Commun. 2001 Nov 9;288(4):1047-51. doi: 10.1006/bbrc.2001.5870.
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