期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 448, 期 1-2, 页码 335-347出版社
SPRINGER
DOI: 10.1007/s11010-018-3392-y
关键词
Maresin 1; Peroxisome proliferator-activated receptor alpha; Oxygen-regulated protein 150; Inflammation; Apoptosis; Atherosclerosis
类别
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) grant - Korea government Ministry of Education [2017R1D1A1B03028892]
- Ministry of Science, ICT, and Future Planning [2016R1C1B2012674]
The current study was designed to investigate the therapeutic effects of Maresin 1 (MAR1) on atherosclerotic response. Human monocytes THP-1 and human umbilical vein endothelial cells (HUVECs) were used to investigate the effects of MAR1 on lipopolysaccharide (LPS)-induced inflammation and apoptosis. In this study, we found that MAR1 induces peroxisome proliferator-activated receptor alpha (PPAR alpha) expression. We also demonstrated that MAR1 suppresses atherosclerotic reactions caused by LPS treatment via a PPAR alpha-dependent pathway. MAR1 treatment inhibited LPS-induced phosphorylation of nuclear factor kappa B (NF-kappa B) and secretion of pro-inflammatory cytokines in HUVECs and THP-1 cells. In HUVEC cells, expression of adhesion molecules and LPS-stimulated adhesion of THP-1 cells to the endothelium were significantly decreased after MAR1 treatment. Furthermore, LPS-induced endoplasmic reticulum (ER) stress and cell apoptosis was significantly decreased after MAR1 treatment of HUVECs. MAR1 also led to a dose-dependent increase in oxygen-regulated protein 150 (ORP150) expression which is responsible for the inhibition of ER stress. Notably, all of the pro-atherosclerotic effects were completely abrogated by treatment with small interfering (si) RNA targeting PPAR alpha. In conclusion, MAR1 ameliorates LPS-induced atherosclerotic reactions via PPAR alpha-mediated suppression of inflammation and ER stress.
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