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. 2020 Oct 22;1:219–232. doi: 10.1016/j.jvssci.2020.09.005

Fig 3.

Fig 3

Effect of K-134 on abdominal aortic aneurysm (AAA) pathology. Treatment with K-134 suppressed medial elastin degradation, macrophage accumulation, and reactive oxygen species (ROS) production at day 28 (pretreatment protocol). Comparisons among the sham (n = 3), K-134(-) group (n = 13), and K-134 (+) groups (n = 20) are shown. Scale bar = 100 μm. L, lumen. T, thrombus. ∗P < .05 vs sham; #P < .05 vs K-134(-). A, Representative images of elastin. Medial elastic disruption was scored as mild (1), high (3), and severe (4). B, Representative images of immunofluorescence staining for macrophage (indicated by green and arrows) and 4′, 6-diamidino-2-phenylindole (DAPI) (blue). Merged images showed that macrophage was accumulated in the media and adventitia. The number of macrophages (CD68+ cells) was counted on each aortic section. C, Representative images of ROS activity (indicated by green) and DAPI (blue). Merged images showed that K-134 treatment significantly decreased ROS activity in the hypoperfusion-induced AAA rat model.