Abstract:

Abstract：Objective To investigate whether intracellular adhesion molecule-1（ICAM-1）could be mediated by nuclear factor-κB（NF-κB）pathway in endothelial cells treated by P. gingivalis W83. Methods As we know production of ICAM-1 in endothelial cells could be increased by infection with P.gingivalis. Then the in vitro models of vascular endothelial cell infected with P. gingivalis W83 was established. Expression of ICAM-1 was examined by Real-time PCR and Western blotting in endothelial cells pretreated with P. gingivalis W83 for 8 h with or without the NF-κB antagonist MG132 at concentration of 5，10，20 μmol/L respectively for 15，30，60 min. SAS 8.12 software was used for statistical analysis；analysis of variance was done to compare the means. Results ICAM-1 production in endothelial cells increased by infection with P.gingivalis，MG132 could abrogate the production of ICAM-1 mRNA at concentration of 10 μmol/L for 30 min，and the production of ICAM-1 was abrogated by MG132 at concentration of 20 μmol/L for 15 min；in addition，the abrogation was more obvious at 30 and 60 min. Conclusion The induction of ICAM-1 by infection with P. gingivalis might be mediated by the NF-κB pathway in endothelial cells.

摘要：

目的 探讨核转录因子-κB（NF-κB）/抑制因子κB（IκB）信号通路在调控牙龈卟啉单胞菌（P. gingivalis）感染诱导血管内皮细胞细胞间黏附分子-1（ICAM-1）高表达过程中的作用。方法 本研究于2008年3月至2011年1月在中国医科大学中心实验室及中国医科大学口腔医学院中心实验室进行。已知P. gingivalis感染血管内皮细胞可诱导其ICAM-1基因和蛋白表达增高。采用Real-time PCR和Western blot法检测P. gingivalis感染后血管内皮细胞ICAM-1 mRNA和蛋白表达；应用5、10、20 μmol/L的蛋白酶体抑制剂MG132分别预处理血管内皮细胞15、30、60 min，再将细胞与P. gingivalis共同培养8 h，观察细胞ICAM-1 mRNA和蛋白表达的变化，分析NF-κB/IκB信号通路对ICAM-1表达的调控作用。结果 10 μmol/L MG132预处理30 min，P. gingivalis感染的血管内皮细胞ICAM-1 mRNA表达具有下降趋势；20 μmol/L MG132预处理15 min，P. gingivalis感染的血管内皮细胞ICAM-1表达即开始下降，预处理时间延长至30、60 min，ICAM-1表达下降更趋明显。结论 阻断NF-κB/IκB信号通路可抑制P. gingivalis感染诱导的血管内皮细胞ICAM-1表达。

关键词: 牙龈卟啉单胞菌, 核转录因子-&kappa, B, 细胞间黏附分子-1