李良成, 侯琦, 郭颖, 程桂芳. 氢化可的松抑制人中性粒细胞与滑膜细胞粘附机理研究J. 药学学报, 2001, 36(6): 401-406.
引用本文: 李良成, 侯琦, 郭颖, 程桂芳. 氢化可的松抑制人中性粒细胞与滑膜细胞粘附机理研究J. 药学学报, 2001, 36(6): 401-406.
LI Liang cheng, HOU Qi, GUO Ying, CHENG Gui fang. INHIBITORY EFFECTS OF HYDROCORTISONE ON HUMAN POLYMORPHONUCLEAR LEUKOCYTE ADHESION TO HUMAN SYNOVIAL CELLJ. Acta Pharmaceutica Sinica, 2001, 36(6): 401-406.
Citation: LI Liang cheng, HOU Qi, GUO Ying, CHENG Gui fang. INHIBITORY EFFECTS OF HYDROCORTISONE ON HUMAN POLYMORPHONUCLEAR LEUKOCYTE ADHESION TO HUMAN SYNOVIAL CELLJ. Acta Pharmaceutica Sinica, 2001, 36(6): 401-406.

氢化可的松抑制人中性粒细胞与滑膜细胞粘附机理研究

INHIBITORY EFFECTS OF HYDROCORTISONE ON HUMAN POLYMORPHONUCLEAR LEUKOCYTE ADHESION TO HUMAN SYNOVIAL CELL

  • 摘要: 目的研究氢化可的松对正常人中性粒细胞(PMN)与滑膜细胞(HSC)粘附的作用及其机理.方法MTT比色法检测PMN与HSC的粘附,Cell-ELISA和RT-PCR法检测HSC粘附分子的表达,EMSA研究核转录因子NF-κB的活化.结果氢化可的松可显著抑制50U·mL-1rhTNF-α与IL-1β刺激的HSC与PMN的粘附;显著抑制HSC表面VCAM-1的表达及VCAM-1mRNA表达,但对ICAM-1mRNA的表达无显著影响;同时对TNF-α诱导的NF-κB活化有显著抑制作用.结论氢化可的松显著抑制PMN与HSC的粘附,其作用机理可能是通过抑制NF-κB的活化,进而抑制滑膜细胞中VCAM-1mRNA及蛋白表达而实现的.

     

    Abstract: AIM To investigate the inhibitory effects of hydrocortisone on human polymorphonuclear leukocyte (PMN) adhesion to human synovial cell (HSC), and to explore its mechanism. METHODS MTT colorimetry was used to determine the adhesion effect of PMN to HSC. Cell-ELISA and RT-PCR methods were used to determine the expression of adhesion molecular ICAM-1 and VCAM-1. EMSA method was also used to observe the activity of nucleus transcription factor-κB (NF-κB). RESULTS Hydrocortisone inhibited TNF-α (50 U·mL-1 for 12 hours) and IL-1β (50 U·mL-1 for 12 hours) induced adhesion of PMN to HSC (IC50 2.05×10-6 mol·L-1 and 2.13×10-7 mol·L-1, respectively) in a concentration dependent manner. Adhesion molecular VCAM-1 and ICAM-1 protein and mRNA (rather than ICAM-1) expression in HSC induced by TNF-α (50 U·mL-1) were inhibited significantly by hydrocortisone at 1×10-6 -10-5mol·L-1. The activity of NF-κB was also extensively inhibited by hydrocortisone at 1×10 -6 -10-5mol·L-1. CONCLUSION Hydrocortisone inhibited TNF-α-stimulated PMN HSC adhesion, and expression of VCAM-1 by suppressing the activity of NF-κB.

     

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