AimTo investigate whether Rho kinase inhibitor fasudil inhibits high glucose (HG)-induced cell adhesion to human umbilical vein endothelial cells (HUVEC) and search for its underlying mechanisms.MethodsThe adhesion of monocytes to HUVEC was determined using fluorescence-labeled monocytes.The mRNA and protein levels of vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein 1（MCP-1） were measured using real-time polymerase chain reaction (RT-PCR) and Western blot.The amounts of RhoA, ROCK1, p-MYPT and MYPT were determined using Western blot analysis.ResultsFasudil significantly suppressed HG-induced adhesion of THP-1 to HUVEC in a dose manner: namely by about 33.4% in the presence of low dose (10-6 mmol/L) and by 42.8% in high dose (10-5 mmol/L) at 24 hours (both P<0.05); the same for 12 h.Fasudil significantly suppressed the HG-induced increase of mRNA and protein expression of VCAM-1 and MCP-1 in dose and time manner.HG markedly increased ratio of p-MYPT/MYPT, while fasudil inhibited HG-induced activation of Rho/ROCK pathway.Conclusion The adhesion of monocytes to HUVEC and the expression of VCAM-1and MCP-1 induced by high glucose could be inhibited by fasudil，the same to activation of Rho/ROCK pathway.It suggests that fasudil may represent a new treatment for diabetic vascular injury.