Aim To understand whether lipid peroxidation in endothelial cells (EC) induces the expression of macrophage inflammatory protein-1α (MIP-1α)and vascular cell adhesion molecule-1 (VCAM-1). Methods The cultured human umbilical vein EC were divided at random into experimental groups (cultured in the media containing 1 μmol/L, 5 μmol/L and 10 μmol/L diamide, respectively) and control group (cultured in standard medium without diamide). The EC of all groups were hybridized, insitu, with the digoxigenin-labeled MIP-1α and VCAM-1 cDNA probes. In addition , the total RNA in EC of all groups extracted by the single-step method, and MIP-1α and VCAM-1 mRNA expression in EC was determined by dot blotting analysis. Results Insitu hybridization showed that both the cytoplasm and nuclei of the normal EC expressed MIP-1α and VCAM-1 mRNA, that were granular blue substances. Diamide induced stronger expression of cytokines in a dose dependent manner. Of which, the expression of MIP-1α and VCAM-1 mRNA in EC in 1 μmol/L diamide group was 1.28- and 1.26-fold, in 5 μmol/L diamide group, 1.87- and 1.54-fold, and in 10 μmol/L diamide group, 2.41- and 2.01-fold as much as that in control group, respectively. The analysis of variance showed that there were significant differences between groups (P<0.05). Dot blotting showed that the expression of MIP-1α and VCAM-1 mRNA in 1 μmol/L diamide group was 1.40- and 1.22-fold, in 5 μmol/L diamide group, 1.90- and 1.56-fold , and in 10 μmol/L diamide group, 2.50- and 2.04-fold as much as that of the control group, and the increased expression of both cytokine mRNA was positively correlated with the diamide concentrations. Conclusions Lipid peroxidation injury might induce adhesion of monocytes to the endothelium and migration into subendothelial space through stimulating EC to produce increased MIP-1α and VCAM-1 and may play an important role in the recruitment of monocytes into the intima in atherogenesis.