Objective      To determine the role of ROCK1 in the inhibitory effect of dexamethasone (Dex) on neutrophil release and monocyte adhesion.       Methods      The inhibitory effect of Dex and Fasudil (Fas) on the release superoxide anion (O

2

-

) and myeloperoxidase (MPO) in neutrophil (PMN) after treatment of PMA

and the adhesion ability of U937 cells to human umbilical vein endothelial cells (HUVEC) af

ter the stimulation as same as above mentioned was also determined. The expression and activity of ROCK1 and RhoA were also determined. Furthermore

the effect of glucocorticoid receptor antagonists (mifepristone

M) and protein synthesis inhibitors (cycloheximide

C) on dexamethasone were also evaluated. Cell samples were divided into control group

PMA group

PMA+Dex group

PMA+Dex+M group

PMA+Dex+C group and PMA+Fas group.       Results      Dex inhibited the release O

2

-

and MPO of PMA-stimulated PMN (1.25±0.10 vs 1.95±0.10

1.07±0.06 vs 1.75±0.08

P0.05)

but Fasudil had no this function (P0.05). Dexamethasone and Fasudil inhibited adhesion ability of U937 cells significantly（0.09±0.01 and 0.08±0.01 vs 0.28±0.06

P0.05）. Mifepristone and cycloheximide did not interfere with the effect of Dex.       Conclusion      Dex inhibits the release of neutrophil via non-ROCK1 dependent pathway

and discourages U937 monocyte adhesion in ROCK1 dependent pathway via non-genomic effects.