摘要
目的研究异丙酚对细菌脂多糖(lipopolysaccharide,LPS)刺激之后的脐静脉内皮细胞(Human umbil-ical vein endothelial cells,HUVECs)的核因子kappaB(NF-κB)活性的影响,探讨异丙酚可能的抗炎机制。方法选择3-4代HUVECs进行转板后都加入LPSlug/ml刺激,按刺激的时间和有无加入药物随机分为4组,A1、B1分别为LPS刺激2h对照组和异丙酚25umol/L组,A2和B2组分别为刺激8h的对照组和异丙酚25umol/L组。提取健康志愿者血液中的多形核中性粒细胞(polymorphonuclear neutrophil,PMN),测定PMN与HUVECs的粘附率:免疫细胞化学测定NF-κBP65亚基的核阳性表达细胞百分率。结果B2组的PMN粘附率(39.36±1.76)%与对照组A2(57.93±4.08)%比较都显著降低(P<0.05);NF-κB核阳性细胞率B1组(71.64±2.32)%比对照组A1(80.28±6.24)%,B2组(75.92±4.45)%比对照组A2(81.58±4.68)%显著降低(P<0.05)。结论异丙酚能有效抑制LPS刺激HUVECs后NF-κB活性的增加,抑制PMN与HUVECs的粘附,减轻机体的炎症反应。
Objective To investigate effect of propofol on the nuclear factor-kappa B (NF-KB) activation of endoth cells induced by lipopolysaecharide (LPS). We expect to explore the mechanism of propofol resisting inflammation 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(lug/ml), then, the activity of NF-KB 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, Bl 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 A1 (57.93±4.08)%(P〈0.05).At the two time points, the nuclear expression of NF-KB in propofol treatment 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-KB 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.
出处
《海南医学》
CAS
2008年第12期16-18,共3页
Hainan Medical Journal