Abstract
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.
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ACKNOWLEDGMENTS
This study was supported by the National Natural Sciences Foundation of China (grant numbers 81271905, 81301489, and 81472009), Science and Technology Planning Project of Guangdong Province (2011B031800090), and Medical Scientific Research Foundation of Guangdong Province (A2011374).
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The authors declare no conflicts of interest associated with this study.
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Ma, X., Zhao, JY., Zhao, ZL. et al. Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells. Inflammation 38, 1329–1336 (2015). https://doi.org/10.1007/s10753-014-0104-y
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DOI: https://doi.org/10.1007/s10753-014-0104-y