Abstract | SCOPE: METHODS AND RESULTS: Human monocyticcells (THP-1) were induced into macrophages in an in vitro model. ω3-PUFAs suppressed Lp-PLA2 expression; the suppression induced by docosahexaenoic acid (DHA) was related to reduced inflammation. Tumor necrosis factor-α (TNF-α) was employed to stimulate the phosphorylation of p38 mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB) p65 and Lp-PLA2 expression in macrophages. The stimulation was inhibited by DHA and the anti-inflammatory drug sodium salicylate. Moreover, the stimulation of Lp-PLA2 expression by TNF-α could be suppressed by NF-κB and MAPK pathway inhibitors. Then, chronic inflammation was induced in an in vivo mouse model, resulting in an increase in Lp-PLA2 expression in peripheral blood mononuclear cells (PBMCs) and arteries. This increase was suppressed by ω3-PUFAs. Inhibition of Lp-PLA2 transcription in PBMCs was also observed in ω3-PUFA-enriched swine. CONCLUSION: Our results demonstrate that the protective effects of ω3-PUFAs against cardiovascular events may be related to the suppression of Lp-PLA2 levels.
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Authors | Zhuang Li, Wenzhi Ren, Xiaolei Han, Xingxing Liu, Gangqi Wang, Mingjun Zhang, Daxin Pang, Hongsheng Ouyang, Xiaochun Tang |
Journal | Molecular nutrition & food research
(Mol Nutr Food Res)
Vol. 59
Issue 9
Pg. 1771-9
(Sep 2015)
ISSN: 1613-4133 [Electronic] Germany |
PMID | 26018800
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
Chemical References |
- Anti-Inflammatory Agents
- Fatty Acids, Omega-3
- NF-kappa B
- Tumor Necrosis Factor-alpha
- Docosahexaenoic Acids
- p38 Mitogen-Activated Protein Kinases
- 1-Alkyl-2-acetylglycerophosphocholine Esterase
- PLA2G7 protein, human
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Topics |
- 1-Alkyl-2-acetylglycerophosphocholine Esterase
(genetics, metabolism)
- Animals
- Anti-Inflammatory Agents
(pharmacology)
- Cardiovascular Diseases
(prevention & control)
- Cell Line
- Disease Models, Animal
- Docosahexaenoic Acids
(pharmacology)
- Down-Regulation
- Fatty Acids, Omega-3
(pharmacology)
- Gene Expression Regulation
- Humans
- Leukocytes, Mononuclear
(drug effects, metabolism)
- Macrophages
(drug effects, metabolism)
- Male
- Mice
- Mice, Inbred C57BL
- NF-kappa B
(genetics, metabolism)
- Phosphorylation
- Tumor Necrosis Factor-alpha
(metabolism)
- p38 Mitogen-Activated Protein Kinases
(genetics, metabolism)
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