Figure 7.

Protective effects of nicotinamide against AAA formation were abrogated by Sirt1 inhibition. AngII was infused via osmotic mini-pump in LDLR KO mice treated with or without nicotinamide ± EX-527, a selective Sirt1 inhibitor. (A) AAA incidence (n = 11–19). (B) Aortic diameter (n = 6–19). (C) Aortic Sirt1 activity (n = 2–4). (D) Representative histology; VVG (elastin fragmentation), MPO, and Mac-3 (macrophages). (E) Pro-inflammatory gene (MCP-1, left panel and TNFα, right, n = 6–9) expression. Data were analysed using one-way ANOVA followed by Bonferroni post-hoc analysis. AngII, angiotensin II; L, lumen; Mac, macrophage; MCP-1, monocyte chemoattractant protein 1; MPO, myeloperoxidase; Nam, nicotinamide; TNFα, tumour necrosis factor α; VVG, Verhoeff-van Gieson.