Abstract: Objective To investigate the effect and mechanisms of rosuvastatin in lipopolysaccharide(LPS) induced late outgrowth endothelial progenitor cells (LOCs) injury. Methods Mononuclear cells were isolated from human peripheral blood by density gradient centrifugation and cultured to obtain the LOCs. Attached cells were divided into control group, LPS treated group and rosuvastatin with different concentration plus LPS groups. CCK-8 was used to measure the cell viability. Malondialdehyde(MDA), lactate dehydrogenase(LDH) and superoxide dismutase(SOD) were detected by colorimetric assay kits. Flow cytometry was used to analyze the production of reactive oxygen species(ROS). Enzyme-linked immuno sorbent assay was utilized to detect the protein levels of IL-6 and IL-8. Western blot was used to determine the TLR4 expression level and the transcription factor assay kit was used to measure the activity of NFκB p65. Results Rosuvastatin could effectively inhibit the decrease of cell viability（P<0.05） induced by LPS and reduce the level of MDA（P<0.05）, LDH（P<0.05）, ROS（P<0.01）, increase the activity of SOD（P<0.05）, decrease the expression level of IL-6 and IL-8（P<0.01）. Moreover, the overexpression of TLR4 and the activation of NFκB p65 induced by LPS were both attenuated by rosuvastatin（P<0.05，P<0.01）. Conclusions Rosuvastatin can significantly increase LOCs viability, decrease the production level of ROS, reduce the oxidative damage and inhibit IL-6 and IL-8 expression in LOCs induced by LPS. The mechanisms may be associated with TLR4/ NFκB p65signaling pathway.

Key words: Rosuvastatin, late outgrowth Endothelial progenitor cells, Oxidative stress, Lipopolysaccharide