ACE2 and Ang-(1-7) significantly inhibit early atherosclerotic lesion formation via protection of endothelial function and inhibition of inflammatory response.

Background and Objectives. Curcumin has long been used to treat age-related diseases, such as atherosclerosis and coronary heart disease. In this study, we explored the effects of curcumin on the development of abdominal aortic aneurysm (AAA). Methods. ApoE−/− mice were randomly divided into 3 groups: AngII group, AngII + curcumin (AngII + Cur) group (100 mg/kg/d), and the control group. Miniosmotic pumps were implanted subcutaneously in ApoE−/− mice to deliver AngII for 28 days. After 4-week treatment, abdominal aortas with AAA were obtained for H&E staining, immunohistochemistry, and Western blotting. Results. The results showed that curcumin treatment significantly decreased the occurrence of AAA. The levels of macrophage infiltration, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factors-α (TNF-α) were significantly lower in AngII + Cur group than those in AngII group (all P < 0.01). The level of superoxide dismutase (SOD) was significantly higher in AngII + Cur group than those in AngII group (P < 0.01). The ERK1/2 phosphorylation in AngII + Cur group was significantly lower than that in AngII group (P < 0.01). Conclusions. These results suggested that curcumin can inhibit the AngII-induced AAA in ApoE−/− mice, whose mechanisms include the curcumin anti-inflammation, antioxidative stress, and downregulation of ERK signaling pathway.