2008Hainan yixueRequires access

Effects of propofol on activation of nuclear fator-kappa B of HUVECs by lipopolysaccharide

Min Liang

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Abstract

Objective To investigate effect of propofol on the nuclear factor-kappa B(NF-κB) activation of endoth cells induced by lipopolysaccharide(LPS).We expect to explore the mechanism of propofol resisting in-flammation at the level of regulation of gene translation.Methods Human umbilical vein endothelial cells(HUVECs) cultured in vitro was randomly divided into four groups.Each group was treated with LPS(1ug/ml),then,the activity of NF-κB B of HUVECs and the ratio of polymorphonuclear neutrophil-endothelial adherence was measured at various time points.For 2 hours treated with LPS,A1 group was control group and A2 group owned propofol 25mmol/L.For 8 hours treated with LPS,B1 group was control group and B2 group was propofol 25mmol/L group.Results The ratio of PMN-endothelial adherence of B2 group(39.36±1.76)% were lower than those of A2(57.93±4.08)%(P0.05).At the two time points,the nuclear expression of NF-κB in propofol treat-ment groupsB1(71.64±2.32)% and B2(75.92±4.45)% was lower than control groupsA1(80.28±6.24)% and A2(81.58±4.68)] espectively.Conclusion Propofol can depress activity of NF-κB of HUVECs were insuiled by LPS and gene translation of ICAM-1.Accordingly,expression of ICAM-1 decreased and ability of PMN-Endothelial adherence was weakened.

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Objective To investigate effect of propofol on the nuclear factor-kappa B(NF-κB) activation of endoth cells induced by lipopolysaccharide(LPS).We expect to explore the mechanism of propofol resisting in-flammation at the level of regulation of gene translation.Methods Human umbilical vein endothelial cells(HUVECs) cultured in vitro was randomly divided into four groups.Each group was treated with LPS(1ug/ml),then,the activity of NF-κB B of HUVECs and the ratio of polymorphonuclear neutrophil-endothelial adherence was measured at various time points.For 2 hours treated with LPS,A1 group was control group and A2 group owned propofol 25mmol/L.For 8 hours treated with LPS,B1 group was control group and B2 group was propofol 25mmol/L group.Results The ratio of PMN-endothelial adherence of B2 group(39.36±1.76)% were lower than those of A2(57.93±4.08)%(P0.05).At the two time points,the nuclear expression of NF-κB in propofol treat-ment groupsB1(71.64±2.32)% and B2(75.92±4.45)% was lower than control groupsA1(80.28±6.24)% and A2(81.58±4.68)] espectively.Conclusion Propofol can depress activity of NF-κB of HUVECs were insuiled by LPS and gene translation of ICAM-1.Accordingly,expression of ICAM-1 decreased and ability of PMN-Endothelial adherence was weakened.

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Available abstract

Objective To investigate effect of propofol on the nuclear factor-kappa B(NF-κB) activation of endoth cells induced by lipopolysaccharide(LPS).We expect to explore the mechanism of propofol resisting in-flammation at the level of regulation of gene translation.Methods Human umbilical vein endothelial cells(HUVECs) cultured in vitro was randomly divided into four groups.Each group was treated with LPS(1ug/ml),then,the activity of NF-κB B of HUVECs and the ratio of polymorphonuclear neutrophil-endothelial adherence was measured at various time points.For 2 hours treated with LPS,A1 group was control group and A2 group owned propofol 25mmol/L.For 8 hours treated with LPS,B1 group was control group and B2 group was propofol 25mmol/L group.Results The ratio of PMN-endothelial adherence of B2 group(39.36±1.76)% were lower than those of A2(57.93±4.08)%(P0.05).At the two time points,the nuclear expression of NF-κB in propofol treat-ment groupsB1(71.64±2.32)% and B2(75.92±4.45)% was lower than control groupsA1(80.28±6.24)% and A2(81.58±4.68)] espectively.Conclusion Propofol can depress activity of NF-κB of HUVECs were insuiled by LPS and gene translation of ICAM-1.Accordingly,expression of ICAM-1 decreased and ability of PMN-Endothelial adherence was weakened.

Key concepts: Medicine, Propofol, Lipopolysaccharide, Umbilical vein, Endothelial dysfunction, In vitro, Immunology, Pharmacology

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