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Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM
Xin Ma1, Jia-Yi Zhao, Zhen-Long Zhao
1Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
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.
Insights
Propofol reduces inflammation by decreasing monocyte chemoattractant protein-1 (MCP-1) production in liver cells. This effect is mediated by increasing apolipoprotein M (apoM) and forkhead box protein A2 (foxa2) expression.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- Monocyte chemoattractant protein-1 (MCP-1) is a key cytokine in inflammatory responses.
- Propofol has demonstrated anti-inflammatory properties, inhibiting pro-inflammatory cytokine production.
- The specific mechanisms by which propofol affects MCP-1 expression are not fully understood.
Purpose of the Study:
- To investigate the effect of propofol on MCP-1 expression in lipopolysaccharide (LPS)-stimulated HepG2 cells.
- To elucidate the underlying molecular mechanisms, including the roles of apolipoprotein M (apoM) and forkhead box protein A2 (foxa2).
Main Methods:
- HepG2 cells were stimulated with LPS and treated with propofol (50 μM) for varying durations (0, 6, 12, 24 h).
- MCP-1 mRNA and protein levels were quantified using real-time quantitative PCR and Western blot analysis.
- The impact of apoM and foxa2 was assessed using small interfering RNA (siRNA) knockdown.
Main Results:
- Propofol significantly reduced MCP-1 mRNA and protein levels in a time-dependent manner.
- Propofol treatment increased the expression of apoM and foxa2 in HepG2 cells.
- siRNA-mediated knockdown of apoM and foxa2 abolished the inhibitory effect of propofol on MCP-1 production.
Conclusions:
- Propofol attenuates LPS-induced MCP-1 production in HepG2 cells.
- This inhibitory effect is achieved by enhancing the expression of apoM and foxa2.
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