Eicosapentaenoic Acid-Enriched Phosphatidylcholine Mitigated Aβ1-42-Induced Neurotoxicity via Autophagy-Inflammasome Pathway
Wen M, Ding L, Zhang L, Zhang T, Teruyoshi Y, Wang Y, Wang Y, Xue C
Journal of agricultural and food chemistry · 34 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- University or hospital
- Open Project of Shandong Collaborative Innovation Center for Antibody Drugs
- Government
- Japan Society for the Promotion of Science
- Government
- National Key Research and Development Program of China
- Government
- Fundamental Research Funds for the Central Universities
- Government
- National Natural Science Foundation of China-Shandong Joint Fund for Marine Science Research Centers
- University or hospital
- Doctoral Foundation of Liaocheng University
- Government
- National Key R&D Program of China
- Grants
- Open Project of Shandong Collaborative Innovation Center for Antibody Drugs (CIC-AD1842); Fundamental Research Funds for the Central Universities (Grant No. 201762028); Japan Society for the Promotion of Science (16K00890); National Natural Science Foundation of China-Shandong Joint Fund for Marine Science Research Centers (U1606403); National Key Research and Development Program of China (2018YFD0901103)
Based on 7 listed funder(s).
Publication
- Published
- 2019-11-14 · J Agric Food Chem · vol. 67 · issue 49 · pp. 13767–13774
- Publisher
- American Chemical Society
- Cited
- 39 citations · more than 92% of similar papers · 3.3× the field average
- Impact
- Top 10% most cited in its field
- References
- 50 works
- Access
- Paywalled
- Research areas
- Fatty Acid Research and Health · Advanced Glycation End Products research · Cholesterol and Lipid Metabolism
- Keywords
- Inflammasome, Neurotoxicity, Eicosapentaenoic acid, Neuroinflammation, Docosahexaenoic acid, Pharmacology, Autophagy, Chemistry, Neuroprotection, Biochemistry, Cell biology, Biology, Inflammation, Polyunsaturated fatty acid, Receptor, Immunology, Fatty acid, Toxicity
- MeSH
- hippocampus, animals, humans, rats, rats, sprague-dawley, alzheimer disease, eicosapentaenoic acid, phosphatidylcholines, memory, autophagy, male, amyloid beta-peptides, inflammasomes
7 authors
From CN, JP
- Min WenLiaocheng University
- Lin DingOcean University of China
- Lingyu ZhangOcean University of China
- Tiantian ZhangOcean University of China
- Teruyoshi YanagitaSaga University
- Yuming Wang · correspondingQingdao National Laboratory for Marine Science and Technology; Ocean University of China
Abstract
Recent studies indicated that neuroinflammation contributes to the exacerbation of Alzheimer's disease (AD) and plays an important role in AD. The NOD-like receptor protein 3 (NLRP3) inflammasome, which is an important component of innate immune system, is associated with a wide range of human central nervous system disorders, including AD. Most of the studies focus on the protective effects of docosahexaenoic acid (DHA) in AD, but eicosapentaenoic acid (EPA) has rarely been involved. Here, we investigate the effects of EPA in the forms of phosphatidylcholine (EPA-PC) and ethyl esters (EPA-EE) in improving Aβ1-42-induced neurotoxicity. The spatial memory ability and the biochemical changes in the hippocampus were measured, including glial cell activation, tumor necrosis factor α production, NLRP3 inflammasome activation, and autophagic flux. The present results showed that the AD rats were significantly protected from spatial memory loss by the supplementation (EPA + DHA = 60 mg/kg, i.g., 20 days) of EPA-PC, while EPA-EE showed no significant benefit. Further mechanism studies suggested that EPA-PC could inhibit Aβ-induced neurotoxicity by alleviating NLRP3 inflammasome activation and enhancing autophagy. These findings indicate that EPA could improve cognitive deficiency in Aβ1-42-induced AD rats via autophagic inflammasomal pathway and the bioactivity differs in its molecular form.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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