Figure 4: Administration of RvD1 to mice with established atherosclerosis suppresses lesional ROS and necrosis and enhances efferocytosis. | Nature Communications

Figure 4: Administration of RvD1 to mice with established atherosclerosis suppresses lesional ROS and necrosis and enhances efferocytosis.

From: An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques

Figure 4

(a) Representative images of DHE and quantification of immunoreactive NOX2 and DHE in aortic root lesions of 8-week and 17-week WD-fed Ldlr−/− mice given vehicle control (Veh) or RvD1 for weeks 12–17 (Fig. 3). Scale bar, 100 μm. Data are shown as mean±s.e.m., one-way ANOVA with Tukey's multiple comparison test, ***P<0.001 early lesions versus other groups. ^^P<0.01 Veh versus RvD1 groups, n=8 for early lesions, n=11 for advanced lesions, n=10 for advanced lesions/RvD1 group. (b) Representative images and quantification of lesional necrosis in the two cohorts of mice. Scale bar, 100 μm. (c) Representative images and quantification of lesional efferocytosis, quantified as the ratio of TUNEL+ apoptotic cells (red) associated with lesional macrophages (green) versus apoptotic cells not associated with macrophages (‘free’). Yellow indicates red/green overlap, and blue indicates DAPI-stained nuclei. Scale bar, 5 μm. Data are shown as mean±s.e.m., t-test, *P<0.05, **P<0.01, n=11 for Veh group and n=10 for RvD1 group.

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