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Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment

Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer’s disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapenta...

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Autores principales: Choi, Ji Yeon, Jang, Jun Sung, Son, Dong Ju, Im, Hyung-Sik, Kim, Ji Yeong, Park, Joung Eun, Choi, Won Rak, Han, Sang-Bae, Hong, Jin Tae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751157/
https://www.ncbi.nlm.nih.gov/pubmed/29182579
http://dx.doi.org/10.3390/ijms18122554
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author Choi, Ji Yeon
Jang, Jun Sung
Son, Dong Ju
Im, Hyung-Sik
Kim, Ji Yeong
Park, Joung Eun
Choi, Won Rak
Han, Sang-Bae
Hong, Jin Tae
author_facet Choi, Ji Yeon
Jang, Jun Sung
Son, Dong Ju
Im, Hyung-Sik
Kim, Ji Yeong
Park, Joung Eun
Choi, Won Rak
Han, Sang-Bae
Hong, Jin Tae
author_sort Choi, Ji Yeon
collection PubMed
description Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer’s disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). We examined whether krill oil diet (80 mg/kg/day for one month) prevents amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections in AD mice model and found that krill oil treatment inhibited the LPS-induced memory loss. We also found that krill oil treatment inhibited the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and decreased reactive oxygen species (ROS) and malondialdehyde levels. Krill oil also suppresses IκB degradation as well as p50 and p65 translocation into the nuclei of LPS-injected mice brain cells. In association with the inhibitory effect on neuroinflammation and oxidative stress, krill oil suppressed amyloid beta (1–42) peptide generation by the down-regulating APP and BACE1 expression in vivo. We found that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) dose-dependently decreased LPS-induced nitric oxide and ROS generation, and COX-2 and iNOS expression as well as nuclear factor-κB activity in cultured microglial BV-2 cells. These results suggest that krill oil ameliorated impairment via anti-inflammatory, antioxidative, and anti-amyloidogenic mechanisms.
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spelling pubmed-57511572018-01-08 Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment Choi, Ji Yeon Jang, Jun Sung Son, Dong Ju Im, Hyung-Sik Kim, Ji Yeong Park, Joung Eun Choi, Won Rak Han, Sang-Bae Hong, Jin Tae Int J Mol Sci Article Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer’s disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). We examined whether krill oil diet (80 mg/kg/day for one month) prevents amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections in AD mice model and found that krill oil treatment inhibited the LPS-induced memory loss. We also found that krill oil treatment inhibited the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and decreased reactive oxygen species (ROS) and malondialdehyde levels. Krill oil also suppresses IκB degradation as well as p50 and p65 translocation into the nuclei of LPS-injected mice brain cells. In association with the inhibitory effect on neuroinflammation and oxidative stress, krill oil suppressed amyloid beta (1–42) peptide generation by the down-regulating APP and BACE1 expression in vivo. We found that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) dose-dependently decreased LPS-induced nitric oxide and ROS generation, and COX-2 and iNOS expression as well as nuclear factor-κB activity in cultured microglial BV-2 cells. These results suggest that krill oil ameliorated impairment via anti-inflammatory, antioxidative, and anti-amyloidogenic mechanisms. MDPI 2017-11-28 /pmc/articles/PMC5751157/ /pubmed/29182579 http://dx.doi.org/10.3390/ijms18122554 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Choi, Ji Yeon
Jang, Jun Sung
Son, Dong Ju
Im, Hyung-Sik
Kim, Ji Yeong
Park, Joung Eun
Choi, Won Rak
Han, Sang-Bae
Hong, Jin Tae
Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title_full Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title_fullStr Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title_full_unstemmed Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title_short Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
title_sort antarctic krill oil diet protects against lipopolysaccharide-induced oxidative stress, neuroinflammation and cognitive impairment
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751157/
https://www.ncbi.nlm.nih.gov/pubmed/29182579
http://dx.doi.org/10.3390/ijms18122554
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