摘要
目的观察活化蛋白C(APC)是否能够通过核因子-κB(NF-κB)途径抑制TNF-α介导的炎症反应。方法分离培养正常组、TNF-ɑ组、TNF-ɑ+rhAPC组的人脐静脉内皮细胞细胞(HUVECs)。用ELISA法,检测细胞上清液中的细胞内粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)及选择素浓度。用逆转录聚合酶链反应、Western bloting技术检测HUVECs NF-κBmRNA、NF-κB蛋白的表达。结果细胞上清液中ICAM-1、VCAM-1及E选择素浓度,TNF-ɑ组较正常组显著升高(均P<0.05);而TNF-ɑ+rhAPC组较TNF-ɑ组显著降低(均P<0.05)。HUVECs NF-κB mRNA、蛋白表达水平,TNF-ɑ组较正常组均显著升高(均P<0.05);而TNF-ɑ+rhAPC组较TNF-ɑ组均显著降低(均P<0.05)。结论 APC通过抑制黏附分子的产生来调节TNF-α介导的炎症反应,其可能是通过NF-κB途径来实现。
Objective To study whether activated protein C can inhibit TNF-α-induced inflammatory response via the NF-κB.Methods Human umbilical vein endothelial cells（HUVECs） were collected and cultured with TNF-ɑ,normal subjects and TNF-ɑ＋ rhAPC group.The protein of intercellular adhesion molecule-1（ICAM-1）,VCAM-1,E-selction in plasma,NF-κB mRNA and protein of NF-κB in HUVECs were detected by enzyme linked immunosorbent assay,reverse transcription polymerase chain reaction,Western bloting,respectively.Results The expression of NF-κB mRNA、NF-κB in peripheral blood mononuclear cells（PBMCs） and the concentration of ICAM-1,VCAM-1,E-selction in supernatants were higher in TNF-ɑ group than those in normal group（all P〈0.05）.By TNF-ɑ＋rhAPC group,the above indexes were decreased significantly compared with those in TNF-ɑgroup（all P〈0.05）.Conclusion Activated protein C ameliorates TNF-α-induced inflammatory response by inhibiting the production of adhesion molecules via the NF-κB.
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2012年第7期528-530,共3页
The Chinese Journal of Clinical Pharmacology
关键词
活化蛋白C
核因子-ΚB
细胞因子
黏附分子
activate protein C； nuclear factor-κB； cytokines； adhesion molecules
