Figure 3.

eNOS activation mediated the protection of rosmarinic acid on the endothelial dysfunction induced by H₂O₂ in rat aortic rings. The rat aortic rings were cotreated with eNOS inhibitor L-NAME (2.0 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) (n = 6). (a) The relative endothelium-dependent vasodilation rate after exposure to RA, eNOS inhibitor L-NAME, and H₂O₂ in rat aortic rings. (b) The NBT reduction after exposure to RA, eNOS inhibitor L-NAME, and H₂O₂ in rat aortic rings. Data are presented as the means ± SD (n = 6). ^∗∗P < 0.01 versus the untreated control group; ^##P < 0.01 versus the H₂O₂-treated group; ^$P < 0.05 and ^$$P < 0.01 versus the H₂O₂- and RA-cotreated groups, respectively.