地塞米松抑制U937细胞黏附与吞噬功能的作用机制

Mechanism of dexamethasone inhibiting U937 cell adhesion and phagocytose function

目的探讨地塞米松抑制单核细胞U937黏附和吞噬功能的机制。方法检测体外培养的U937在佛波脂（phorbol-12-myristate-13-acetate，PMA）刺激下分别接受地塞米松和法舒地尔作用后，观察人脐静脉内皮细胞（humanumbilicalveinendothelialcells，HUVEC）黏附和吞噬能力的变化，并检测ROCKl（rho—associatedcoiled—coilproteinkinase1，ROCK1）蛋白含量及其活性的变化；同时观察米非司酮和放线菌酮对地塞米松的影响。结果地塞米松和法舒地尔均可显著抑制受PMA刺激的U937细胞的黏附率和吞噬效果，并抑制ROCK1活性；米非司酮和放线菌酮并不能影响地塞米松抑制U937细胞的黏附和吞噬作用。结论地塞米松能通过抑制U937细胞内ROCK1的活性而干扰其黏附、吞噬功能。

Objective To investigate the mechanism of dexamethasone （Dex） in inhibiting monocyte adhesion and phagocytose function. Methods Under the stimulation of phorbol-12-myristate-13- acetate （PMA） , U937 monocytes cultured in vitro were treated with Dex and Fasudil respectively. The adhesion rate of U937 monocytes to human umbilical vein endothelial cells （HUVECs） and their phago- cytic ability of India ink were studied. The protein content and activity of rho-associated coiled-coil protein kinase 1 （ ROCK1 ） as well as the effects of mifepristone and cycloheximide on Dex were determined. Results Both DEX and Fasudil could significantly inhibit the adhesion rate and phagocytosis of U937 cells stimulated by PMA and suppressed the activity of ROCK1. While mifepristone and cycloheximide could not alter these effects of DEX. Conclusion DEX interferes with the adhesion and phagocytosis function of U937 cells by inhibiting ROCK1 activity.