Objective      To determine the effect of 12-lipoxygenase (12-LO) over-expression on endothelial function and investigate its underlying mechanisms.   Methods      Sprague Dawley rats were randomly divided into sham operation group

balloon injury group (BI)

balloon injury+Lentivirus-GFP group (BI+Lv-GFP)

balloon injury+Lentivirus-12-LO group (BI+Lv-12-LO). Except the rats of sham operation group

all the other rats were inflicted with carotid artery balloon injury operation. BI+Lv-GFP group and BI+Lv-12-LO group were followed by being transfected with lentivirus expressing GFP or 12-LO into the injured artery. In 12 d after transfection

all rats were sacrificed. Intimal hyperplasia was observed using HE staining. The expression of 12-LO was detected by Western blotting. The expression levels of endothelial nitric oxide synthase (eNOS) and intracellular adhesion molecule-1 (ICAM-1) were detected by real time-qPCR

immunohistochemistry and Western blotting.   Results        Lv-12-LO was successfully transfected and expressed in the vascular wall (P0.01). Compared with the sham operation group

the intimamedia thickness (IMT) was increased (P0.01)

the expression of ICAM-1 at mRNA (P=0.001) and protein (P=0.038) levels was elevated

and the expression of eNOS mRNA (P=0.012) and protein (P=0.009) was decreased in the BI group. Compared with the BI+Lv-GFP group

the IMT was increased (P=0.001)

the expression of ICAM-1-mRNA (P=0.009) and protein (P=0.002) was significantly increased

and the expression of eNOS mRNA (P=0.004) and protein (P=0.020) were significantly decreased of BI+Lv-12-LO group. Immunohistochemical assay showed the positive rate of ICAM-1 was higher (P=0.007)

meanwhile the eNOS positive rate was lower in the BI group than the sham operation group (P=0.001). Compared with the BI+Lv-GFP group

the ICAM-1 positive rate was significantly increased (P0.01)

and the eNOS positive rate was significantly decreased (P0.01) in the BI+Lv-12-LO group.     Conclusion    1    2-LO over-expression aggravates the damage of vascular endothelial function by affecting the expression of endothelial factors and inflammatory factors.