ABSTRACT
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 (3. 863 ± 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, (5. 627 ± 330) pg/mL and (1. 626 ± 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.
ABSTRACT
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.
ABSTRACT
Objective:To explore the influence of ischemia/reperfusion (anoxia/reoxygenation)[FK(W16*2。142mmZQ1mm]on immunofunction of endothelial cells(ECs) and effect of intervention with 2-hydroxymethyl-3,5,6-trimethylpyrazine on it.Methods:Model of ECs induced by anoxia/reoxygenation was established to mimic ECs ischemia/reperfusion injury in vivo with human umbilical vein endothelial cell line ECV304.Then 2-hydroxymethyl-3,5,6-trimethylpyraxine was used to intervene the anoxia/reoxygenation process.Nuclear transcriptional factor-?B(NF-?B) was exhibited by fluorescent staining,HLA-ABC,HLA-DR,CD86 and CD54 were detected by flow cytometry.Mixed endothelial cell-lymphocyte reaction(MELR) was conducted to examine the proliferation of lymphocyte,production of IL-2 and percentage of apoptotic lymphocyte.Results:Anoxia/reoxygenation made the ECV304 cell became round,shrunk and abscised,with increased plasma NF-?B,and changed from positive cytoplasm to positive nucleus.HLA-ABC,HLA-DR and CD86 on surface of cells increased but CD54 showed unchanged.MELR showed the incorporation of ~3H-TdR and production of IL-2 increased significantly and the percentage of apoptotic lymphocyte decreased.After 2-hydroxymethyl-3,5,6-trimethylpyrazine intervention,the ECV304 cell shapes recovered,NF-?B expression didn’t down-regulated,but the percentage of positive cells decreased,changes to positve dominant.Besides,reversal changes were shown in other parameters.Conclusion:Anoxia/reoxygenation influences some important immune related molecules in ECV304 cells.2-hydroxymethyl-3,5,6-trimethylpyrazine could antagonize these influences to maintain the immune function of endothelial cells in a relative normal manner.