Aims: 

Statins appear to regulate endothelial nitric oxide synthase expression, thus modulating vasculature. Lipopolysaccharides (LPS) induce endothelial dysfunction through the inhibition of eNOS. The aim of this study was to analyze the molecular and cellular basis of the protective effect of atorvastatin on endothelial cells.

Methods: 

Cultured HUVEC cells were classified in four groups: Group 1: untreated cells (control); Group 2: cells treated with 10 mg/ml of LPS for 6 h; Group 3: cells treated with atorvastatin 1 mM for 6 h; Group 4: cells pre-treated with atorvastatin 1 mM followed by 10 mg/ml of LPS for 6 h. The expression of iNOS and eNOS was measured qRT-PCR. Besides, markers for oxidative/nitrosative stress and mitochondrial damage were also determined.

Results: 

Incubation with 10 mg/ml LPS significantly downregulated the expression of eNOS. Atorvastatin not only counteracted the effect of LPS, but increased the eNOS expression above its basal value. These changes were followed by a normalization of the oxidative stress status of the cells.

Conclusions: 

Our results demonstrated that atorvastatin displays additional protective effects on vasculature, regulating the expression of eNOS. These data support a beneficial action of statins on endothelial function.

Supported by grants: Pfizer, RD06/0013/0008, and CTS-101