NF-κB/IκB信号通路对牙龈卟啉单胞菌感染诱导血管内皮细胞ICAM-1表达调控研究

Influence of nuclear factor-κB/inhibitory κB pathway on intracellular adhesion molecule-1 expression inducedby P. gingivalis in endothelial cells.

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-timePCR和Western blot法检测P.gingivalis感染后血管内皮细胞ICAM-1mRNA和蛋白表达;应用5、10、20μmol/L的蛋白酶体抑制剂MG132分别预处理血管内皮细胞15、30、60min,再将细胞与P.gingivalis共同培养8h,观察细胞ICAM-1mRNA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 10μmol/LMG132预处理30min,P.gingivalis感染的血管内皮细胞ICAM-1mRNA表达具有下降趋势;20μmol/LMG132预处理15min,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、60min,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。

Objective To investigate whether intracellular adhesion molecule-1 （ICAM-1 ）could be mediated by nucle- ar factor-KB （NF-KB）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 endo- thelial 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-~B antagonist MG 132 at concentration of 5,10,20 p.mol/L respectively for 15,30,60 min. SAS 8.12 software was used for statistical anal- ysis;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 p, mol/L for 30 min, and the production of ICAM-1 was abrogated by MG132 at concentration of 20 p.mol/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. gingiva- lis might be mediated by the NF-KB pathway in endothelial cells.