Figure 4.

AMPK activation mediated the protection of rosmarinic acid against the endothelial dysfunction induced by H₂O₂ in rat aortic rings. The rat aortic rings were cotreated with AMPK activator AICAR (50 μM, 10 min) or inhibitor compound C (10 μM) and RA (50 μM) for 10 min, then exposed to H₂O₂ (5.0 mM) for another 10 min. The endothelial function was assessed by the endothelium-dependent vasodilation induced by acetylcholine (ACh, 10 μM). (a) The relative endothelium-dependent vasodilative rate after exposure to RA, AMPK modulator, and H₂O₂ in rat aortic rings. (b) The NBT reduction after exposure to RA, AMPK modulator, and H₂O₂ in rat aortic rings. Data are presented as the means ± SD (n = 6). ^∗P < 0.05 versus the untreated control group; ^∗∗P < 0.01 versus the untreated control group; ^##P < 0.01 versus the H₂O₂-treated group; ^$$P < 0.01 versus the H₂O₂- and RA-cotreated groups.