Research Paper Volume 15, Issue 24 pp 15196—15212

Macrophage-specific deletion of Notch-1 induced M2 anti-inflammatory effect in atherosclerosis via activation of the PI3K-oxidative stress axis

class="figure-viewer-img"

Figure 1. Notch-1 was significantly increased in the human vulnerable atherosclerotic lesion. (A) Representative images of the human vulnerable atherosclerotic lesion and stable lesion. In the representative images of the human vulnerable atherosclerotic lesion, thinning of fibrous caps, enlargement of lipid core and necrotic sites, and macrophage increase could be observed. (B) Western blotting and quantitative analysis revealed that the Notch-1 expression was significantly enhanced in the human vulnerable atherosclerotic lesion. **P < 0.01: human vulnerable atherosclerotic lesion vs. stable lesion. (C) Immunofluorescence microscopy, and quantitative analysis revealed increased immunofluorescence of Notch-1 and iNOS in macrophages of the human vulnerable atherosclerotic lesion compared with the stable lesion. **P < 0.01: human vulnerable atherosclerotic lesion vs. stable lesion.