A comparative study of EPA-enriched ethanolamine plasmalogen and EPA-enriched phosphatidylethanolamine on A42 induced cognitive deficiency in a rat model of Alzheimer's disease

被引：70

作者：

Che, Hongxia ^{[1
]}

Li, Qian ^{[1
]}

Zhang, Tiantian ^{[1
]}

Ding, Lin ^{[1
]}

Zhang, Lingyu ^{[1
]}

Shi, Haohao ^{[1
]}

Yanagita, Teruyoshi ^{[2
]}

Xue, Changhu ^{[1
,3
]}

Chang, Yaoguang ^{[1
]}

Wang, Yuming ^{[1
,3
]}

机构：

[1] Ocean Univ China, Coll Food Sci & Engn, Qingdao 266003, Shandong, Peoples R China

[2] Nishikyushu Univ, Dept Hlth & Nutr Sci, Kanzaki, Japan

[3] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Drugs & Biol Prod, Qingdao 266237, Shandong, Peoples R China

来源：

FOOD & FUNCTION | 2018年 / 9卷 / 05期

基金：

中国国家自然科学基金;

关键词：

NEURONAL APOPTOSIS; LEARNING-ABILITY; OXIDATIVE STRESS; PHOSPHOLIPIDS; BETA; PROTECT; BRAIN; MICE;

D O I：

10.1039/c8fo00643a

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Ethanolamine plasmalogen (pPE), a major phospholipid in neuronal membranes, is specifically reduced in postmortem brains from patients with Alzheimer's disease (AD). The purpose of the present study was to compare the effects of EPA-enriched ethanolamine plasmalogen (EPA-pPE) and EPA-enriched phosphatidylethanolamine (EPA-PE) on cognitive deficiency and illustrate the possible underlying mechanisms. SD rats were divided into four groups including the sham group injected with 0.9% saline and three amyloid- (A) infusion groups, A42 group, EPA-pPE group and EPA-PE group. EPA-pPE and EPA-PE were administered by gavage (150 mg kg(-1) day(-1)), respectively, once a day for 26 days. Administration of EPA-pPE exerted better effects than EPA-PE in improving A-induced cognitive deficiency in a rat model of Alzheimer's disease. Further mechanical research indicated that EPA-pPE was superior to EPA-PE in regulating oxidative stress via increasing SOD activity and decreasing MDA level, as well as reducing GSK-3 and tau phosphorylation. Moreover, EPA-PE was more effective than EPA-pPE at inhibiting the protein expressions of Bax and caspase 9. The results of neuro-inflammation and inflammasome activation showed that EPA-pPE exerted more significant effects than EPA-PE in inhibiting the expressions of TNF- and IL-1, and decreasing NLRP3, pro-caspase 1 and caspase 1 levels. EPA-pPE alleviated A-induced neurotoxicity by inhibiting oxidative stress, neuronal injury, apoptosis and neuro-inflammation, which might depend on the vinyl ether linkage at the sn-1 position.

引用

页码：3008 / 3017

页数：10

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