Aim To investigate whether lipid peroxidation injury to cultured endothelial cells (ECs) induces the expression of macrophage inflammatory protein-1α(MIP-1α). Methods The cultured human umbilical vein ECs were randomly divided into the A,B and C groups,cultured in the media containing 1 μmol/L,5 μmol/L and 10 μmol/L diamide respectively and the control group cultured in the media without diamide.After exposure of ECs to diamide for 4 h,the lipopeeroxide in the ECs was determined by thiobarbiuric acid flurophotometry;toral cellular RNA was extracted from the culrured ECS by the single step method, amd the expression of MIP-1α mRNA was determined by RT-PCR;the MIP-1α protein in ECs was determined by immunocytochemistry. Results The malomdialdehyde content in ECs im group A,B and C were 2.0-fold and 8.6-fold as much as that there was significant difference between experiment group and control group (F=138.64,P<0.01), and Q test also revealed statistical difference among the experiment groups (P<0.05). RT-PCR showed that the MIP-1α mRNA expression in ECs im group A, B and C were 4-fold, 6-fold and 3.5-fold as much as that in the control group. Immunocytochemistry assay showed that MIP-1α mRNA Protein was granular brown substance which located mainly in the cytoplasm around the nuclei.Diamide induced stronger expression of MIP-1α protein in the experimental groups. Image analysis showed that the expression of MIP-1α protein in ECs was 1.9-fold B,1.4-fold in group A and 1.3-fold in group C as mush as that in the control group.The analysis of variance proved that there were significant differences between the experimental groups and the control group (F=68.60,P<0.01),and there were also significant differences among group A,B and C which were proved by Q test (P<0.05). Conclusion Lipid peroxidation injury may play an important role in recuitment of monocytes into intima in atherogenesis through inducing ECs to produce increased MIP-1α.