摘要
目的:探讨地氟醚预处理对于核因子(NF)-κB信号转导通路激活后效应分子的影响。方法:选用人脐静脉内皮细胞株(ECV304)。将细胞分为5组:(1)空白对照组;(2)缺氧/复氧(A/R)组;(3)A/R+肿瘤坏死因子-α(TNF-α,10ng.mL-1)刺激组(A/R+TNF-α组);(4)地氟醚1.0MAC预处理+A/R组(Des+A/R组);(5)地氟醚1.0MAC预处理+A/R+TNF-α(10ng.mL-1)刺激组(Des+A/R+TNF-α组)。应用逆转录-聚合酶链反应(RT-PCR)法分别检测各组细胞的细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)和白细胞介素-8(IL-8)的基因表达水平。结果:A/R组较对照组细胞的ICAM-1、VCAM-1和IL-8mRNA表达水平均有所增加;而经地氟醚预处理后,Des+A/R组细胞的mRNA表达较A/R组有明显降低。结论:地氟醚预处理可抑制TNF-α刺激的内皮细胞表面黏附分子及炎性介质的基因表达水平。
Objective:To evaluate the effect of activated NF-κB signal transduction pathway induced by anoxia/reoxygenation injury.Methods: This study was based on human umbilical vein endothelial cell line(ECV304).The ECV304 cells were divided into 5 groups,the control group,A/R group,A/R + TNF-α 10ng·mL-1 group,Des + A/R group,and Des + A/R + TNF-α 10ng·mL-1 group.The gene expression of intercellular adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1) and interleukin-8(IL-8) was detected by reverse transcription-polymerase chain reaction(RT-PCR).Results: In A/R group,the expression was higher than that in control group,significantly increased in A/R+TNF-α group,but significantly decreased in Des+A/R group and Des+A/R+TNF-α group.Conclusions: Desflurane preconditioning could inhibit the expression levels of inflammatory mediators and adhesion molecules induced by anoxia/reoxygenation injury.
出处
《中国临床医学》
2010年第3期403-404,共2页
Chinese Journal of Clinical Medicine