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Effect of propofol on generation of inflammatory mediator of monocytes
Yun Nie1, Yan-Xi Lu1, Li-Hong Lv1
1Operating Room, First People's Hospital of Ji'nan, Shandong 250011, China.
Objective:
To evaluate the effect of propofol with different concentrations on the expression of inflammatory mediators of interleukin and tumor-necrosis factor-α (TNF-α) by stimulating the mouse primary monocytes and human monocytic cell line with lipopolysaccharide (LPS) and also discuss the effect of propofol on the secretion of inflammatory mediator and its possible molecular mechanism.
Methods:
The mononuclear cells of mouse spleen were separated and then purified to obtain the primary monocytes. The dose-effect relationship of production of pro-inflammatory cytokines by monocytes which were stimulated by LPS, namely the monocytes were stimulated by the dose of 0-500 ng/mL for 24 h. ELISA was employed to detect the concentration of IL-6, IL-8 and TNF-α. The effect of propofol on the secretion of above pro-inflammatory cytokines by the monocytes was observed. Cells were divided into the control group, the 0.1% DMSO group, the LPS group and the treatment group with LPS + different dose of propofol (propofol 1-100 μg/mL). ELISA was employed to detect the concentration of IL-6, IL-8 and TNF-α. The change in the expression of important signaling molecules in Toll-like receptor and NF-κB signaling pathway was detected after THP-1 cells were treated with propofol.
Results:
The concentration of TNF-α was (3863 ± 153) pg/mL after 12 h of stimulation by LPS and then its concentration was decreased gradually. But the concentration of IL-6 and IL-8 was relatively high after 24 h of stimulation by LPS, (5627 ± 330) pg/mL and (1626 ± 200) pg/mL, respectively. The propofol could inhibit the expression of IL-6, IL-8 and TNF-α caused by LPS. After the intervention treatment of 50 μg/mL propofol, the concentration of IL-6, IL-8 and TNF-α was significantly decreased (P < 0.01).
Conclusions:
The propofol can inhibit the expression of TLR-4 and NF-κB to inhibit the activation of p38 and the expression of pro-inflammatory cytokines.
Insights
Propofol effectively inhibits the expression of inflammatory mediators like interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) in monocytes stimulated by lipopolysaccharide (LPS). This suggests propofol
Area of Science:
- Immunology
- Pharmacology
Background:
- Lipopolysaccharide (LPS) is a potent stimulator of inflammatory responses in monocytes.
- Interleukin-6 (IL-6), IL-8, and tumor necrosis factor-alpha (TNF-α) are key pro-inflammatory cytokines involved in immune responses.
- Propofol is a widely used anesthetic agent with potential immunomodulatory effects.
Purpose of the Study:
- To investigate the impact of varying propofol concentrations on the expression of IL-6, IL-8, and TNF-α in LPS-stimulated mouse primary monocytes and human monocytic cell lines.
- To elucidate the molecular mechanisms underlying propofol's effect on inflammatory mediator secretion.
Main Methods:
- Primary monocytes were isolated from mouse spleen and stimulated with LPS (0-500 ng/mL for 24 hours).
- Enzyme-linked immunosorbent assay (ELISA) was used to quantify IL-6, IL-8, and TNF-α concentrations.
- THP-1 cells were treated with LPS and varying concentrations of propofol (1-100 μg/mL) to assess effects on cytokine secretion and signaling pathways (Toll-like receptor and NF-κB).
Main Results:
- LPS stimulation led to significant increases in TNF-α (3863 ± 153 pg/mL at 12h), IL-6 (5627 ± 330 pg/mL at 24h), and IL-8 (1626 ± 200 pg/mL at 24h).
- Propofol treatment significantly inhibited LPS-induced expression of IL-6, IL-8, and TNF-α.
- A concentration of 50 μg/mL propofol markedly reduced the levels of these pro-inflammatory cytokines (P < 0.01).
Conclusions:
- Propofol demonstrates significant anti-inflammatory properties by suppressing the release of key cytokines.
- The mechanism involves the inhibition of Toll-like receptor 4 (TLR-4) and NF-κB signaling pathways.
- This inhibition ultimately reduces the activation of p38 and the subsequent production of pro-inflammatory cytokines.
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