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Propofol reduces lipopolysaccharide-induced, NADPH oxidase (NOX 2) mediated TNF- α and IL-6 production in macrophages
Tao Meng1, Jingya Yu2, Zhen Lei1
1Department of Anesthesiology, Qilu Hospital of Shandong University, Shandong University, No. 107 Wen Hua Xi Road, Jinan, Shandong 250012, China.
Abstract:
During an infection, lipopolysaccharide (LPS) stimulates the production of reactive oxygen species (ROS), which is mediated, in large part, by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs); NOX2 is the major NOX isoform found in the macrophage cell membrane. While the immunomodulatory activity of propofol is highly documented, its effect on the LPS-induced NOX2/ROS/NF-κB signaling pathway in macrophages has not been addressed. In present study, we used murine macrophage cell line RAW264.7 pretreated with propofol and stimulated with LPS. IL-6 and TNF-α expression, ROS production, and NOX activity were determined. Results showed that propofol attenuated LPS-induced TNF-α and IL-6 expression. Moreover, LPS-stimulated phosphorylation of NF-κB and generation of ROS were weakened in response to propofol. Propofol also reduced LPS-induced NOX activity and expression of gp91phox and p47phox. We conclude that propofol modulates LPS signaling in macrophages by reducing NOX-mediated production of TNF-α and IL-6.
Insights
Propofol reduces inflammatory responses in macrophages by inhibiting the lipopolysaccharide (LPS)-induced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) pathway. This inhibition lessens the production of reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6).
Area of Science:
- Immunology and Cell Biology
- Pharmacology and Drug Action
Background:
- Lipopolysaccharide (LPS) infection triggers reactive oxygen species (ROS) production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs), particularly NOX2 in macrophages.
- Propofol's immunomodulatory effects are known, but its impact on the LPS-induced NOX2/ROS/NF-κB pathway in macrophages remains uninvestigated.
Purpose of the Study:
- To investigate the effect of propofol on the LPS-induced NOX2/ROS/NF-κB signaling pathway in murine macrophages.
- To determine propofol's influence on inflammatory cytokine expression (IL-6, TNF-α) and NOX activity.
Main Methods:
- Murine macrophage cell line RAW264.7 was pretreated with propofol and subsequently stimulated with LPS.
- Assessed interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression.
- Measured reactive oxygen species (ROS) production, NOX activity, and expression of NOX subunits (gp91phox, p47phox).
Main Results:
- Propofol significantly attenuated LPS-induced TNF-α and IL-6 expression.
- LPS-stimulated phosphorylation of NF-κB and ROS generation were reduced by propofol.
- Propofol decreased LPS-induced NOX activity and the expression of gp91phox and p47phox.
Conclusions:
- Propofol modulates LPS signaling in macrophages.
- It reduces NOX-mediated production of inflammatory cytokines TNF-α and IL-6.
- This suggests a potential therapeutic role for propofol in managing LPS-induced inflammation.
