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. 2019 Nov 9;116(14):2226–2238. doi: 10.1093/cvr/cvz303

Figure 1.

Figure 1

Niacin protected against AngII-induced AAA formation. AngII was infused via osmotic mini-pump in LDLR KO mice, which were treated with or without niacin in the drinking water. (A) AAA incidence (n = 12–13). (B) Aortic diameter (n = 5–9). (C) Plasma MPO levels (ELISA, n = 3). (D) Representative histology; H&E, MPO, Mac-3 (macrophages), VVG (elastin fragmentation), MMP-2/-9, and MCP-1. (E) Elastin break count (n = 4–6). (F) Representative zymogram (upper panel) and quantified data (bottom panel) for aortic MMP-2 and MMP-9 activities (n = 3–4). (G) mRNA expression of MMP-2 (n = 4–5), MMP-9 (n = 4–5), MCP-1 (n = 4–7), and TNFα (n = 6–7). Data were analysed using one-way ANOVA followed by Bonferroni post hoc analysis. AngII, angiotensin II; H&E, haematoxylin & eosin; L, lumen; Mac, macrophage; MCP-1, monocyte chemoattractant protein 1; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NA, nicotinic acid; TNFα, tumour necrosis factor α; VVG, Verhoeff-van Gieson.