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. 2020 Apr 17;24(10):5911–5925. doi: 10.1111/jcmm.15278

FIGURE 1.

FIGURE 1

Inhibition of nitric oxide (NO) production by L‐NAME abrogates the inhibitory effects of dihydromyricetin (DMY) on atherosclerosis in Apoe− / − mice. A, Lesion areas were quantified by Oil Red O (ORO)‐stained thoracoabdominal aorta. B, Lesion areas were quantified by ORO‐stained aortic sinus sections. Scale: 200 μm. C, D, Representative images and quantification show Mac‐2–positive macrophages (C) and CD4‐positive T cells (D) in the aortic sinus lesions. Scale: 200 μm (C) and 100 μm (D). Arrows indicate CD4‐positve T cells in aortic sinus lesions. E, Representative images and quantification show α‐smooth muscle actin (α‐SMA)‐positive smooth muscle cells (SMCs) accumulation in the aortic sinus lesions. Arrows indicate differential SMCs accumulation in aortic sinus lesions. Scale: 200 μm. F, ELISA analysis of NO levels in plasma from vehicle, DMY or DMY combined with L‐NAME–treated Apoe− / − mice. G, Representative images and quantification show VCAM‐1 expression in endothelial cells in the aortic sinus lesions. Frozen sections of aortic sinus were stained for anti‐VCAM‐1 (green), anti‐CD31 (red) and 4′,6‐diamidino‐2‐phenylindole (DAPI; blue). The dashed line area indicates differential VCAM‐1 expression in endothelial cells. Scale: 100 μm. Data shown are mean ± SEM (n = 7‐10 mice per group). *P < .05