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. 2014 Dec 10;4(1):44–55. doi: 10.5966/sctm.2014-0091

Figure 5.

Figure 5.

MIP-2 restores endothelium-dependent relaxation. High-fat diet-fed apoE−/− mice treated without (PBS, vehicle control) or with MIP-2 (50 μg/kg) were sacrificed at 1 week after treatment. (A): The thoracic aortic rings were isolated freshly for determining the concentration-response curves of acetylcholine-dependent relaxation (n = 5–6 in each group). ∗∗∗, p < .001 MIP-2 versus vehicle control at the indicated concentrations. (B): Representative aortic root microsections show the plaque formation (left). Right: Quantitative data are expressed as percentages of the total luminal surface area of the aorta (n = 3–4 in each group). (C): Immunostaining of phospho-Akt and phospho-eNOS protein expression (left). Representative aortic root sections show phospho-Akt and phospho-eNOS expression in the endothelial lining. Right: Quantitative data are expressed as percentages of immunopositive cells of total endothelial lining cells (n = 3–4 in each group). ∗, p < .05. Scale bars = 500 μm (B), 50 μm (C). Magnification, ×40 (B), ×400 (C). Abbreviations: MIP-2, macrophage inflammatory protein-2; p-Akt, phospho-Akt; PBS, phosphate-buffered saline; p-eNOS, phosphorylated endothelial nitric-oxide synthase.