【摘要】 目的:初步探讨胺酮对脂多糖(Lipopolysaccharides,LPS)作用下人脐静脉内皮细胞(Human umbilical vein endothelialcells,HUVECs)核因子-κB(Nuclear factor-kappa B,NF-κB)易位活化的影响及氯胺酮的抗炎效应。方法:HUVECs分为4组:C组(空白对照组)、L组(加入1μg/ml LPS)、KL1组(3μg/ml的氯胺酮+1μg/ml LPS)、KL2组(30μg/ml的氯胺酮+1μg/ml LPS)。采用免疫印记法(Western blot)、反转录聚合酶链式反应(Reverse transcription polymerase chain reaction,RT-PCR)和HPIAS2000图象分析系统,测定NF-κB p65亚基的易位活化表达。结果:KL1组、KL2组能抑制LPS作用下HUVECs内的NF-κB p65易位表达(P<0.05)。结论:LPS可引起人脐静脉内皮细胞核因子-κB的表达,而氯胺酮可以抑制其作用,且其抑制作用可能与剂量呈正相关。氯胺酮的抗炎机制可能是在核因子-κB转录水平上实现的。更多还原

【Abstract】 Objective:To investigate the effects of Ketamine on lipopolysaccharide(LPS)-induced translocation of nuclear factor-kappaB(NF-κB) in human umbilical vein endothelial cell nuclei and to explore it’s anti-inflammatory action.Methods:Human umbilical vein endothelial cells(HUVECs) were divided into four groups:group C(blank control group),group L(1 μg/ml LPS was added),group KL1(3 μg/ml ketamine and 1 μg/ml LPS were added) and group KL2(30 μg/ml ketamine and 1 μg/ml LPS were added).The tanslocation and expressions of NF-κB p65 in endothelial cell nuclei were detected by Western blot,reverse transcription polymerase chain reaction(RT-PCR) and image analysis system of HPIAS 2000.Results:The tanslocation and expression of NF-κB p65 in endothelial cell nuclei induced by LPS were reduced in group KL1 and KL2.Conclusions:The tanslocation and expression of NF-κB p65 in endothelial cell nuclei can be induced by LPS and Ketamine can suppress the activation.There are positive correlations between Ketamine concentration and its inhibitory effect.The anti-inflammatory effect of Ketamine may be achieved by the translocation of NF-κB.更多还原