Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells

Monocyte chemoattractant protein-1 (MCP-1) is a cytokine that mediates the influx of cells to sites of inflammation. Our group recently reported that propofol exerted an anti-inflammatory effect and could inhibit lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines. However, the...

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Bibliographic Details
Published in:Inflammation 2015-06, Vol.38 (3), p.1329-1336
Main Authors: Ma, Xin, Zhao, Jia-Yi, Zhao, Zhen-Long, Ye, Jing, Li, Shu-Fen, Fang, Hai-Hong, Gu, Miao-Ning, Hu, Yan-Wei, Qin, Zai-Sheng
Format: Article
Language:English
Subjects:
Anesthetics, Intravenous - pharmacology
Anti-Inflammatory Agents - pharmacology
Apolipoproteins - biosynthesis
Apolipoproteins - genetics
Apolipoproteins M
Biomedical and Life Sciences
Biomedicine
Cell Line
Cell Movement
Chemokine CCL2 - biosynthesis
Chemokine CCL2 - genetics
Chemokine CCL2 - metabolism
Hep G2 Cells
Hepatocyte Nuclear Factor 3-beta - biosynthesis
Hepatocyte Nuclear Factor 3-beta - genetics
Humans
Immunology
Internal Medicine
Lipocalins - biosynthesis
Lipocalins - genetics
Lipopolysaccharides
Pathology
Pharmacology/Toxicology
Propofol - pharmacology
Rheumatology
RNA Interference
RNA, Messenger - biosynthesis
RNA, Small Interfering
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Summary:Monocyte chemoattractant protein-1 (MCP-1) is a cytokine that mediates the influx of cells to sites of inflammation. Our group recently reported that propofol exerted an anti-inflammatory effect and could inhibit lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines. However, the effect and possible mechanisms of propofol on MCP-1 expression remain unclear. LPS-stimulated HepG2 cells were treated with 50 μM propofol for 0, 6, 12, and 24 h, respectively. The transcript and protein levels were measured by real-time quantitative PCR and Western blot analyses, respectively. We found that propofol markedly decreased both MCP-1 messenger RNA (mRNA) and protein levels in LPS-stimulated HepG2 cells in a time-dependent manner. Expression of apolipoprotein M (apoM) and forkhead box protein A2 (foxa2) was increased by propofol treatment in HepG2 cells. In addition, the inhibitory effect of propofol on MCP-1 expression was significantly abolished by small interfering RNA against apoM and foxa2 in LPS-stimulated HepG2 cells. Propofol attenuates LPS-induced MCP-1 production through enhancing apoM and foxa2 expression in HepG2 cells.
ISSN:0360-3997
1573-2576
DOI:10.1007/s10753-014-0104-y