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. 2023 Dec 7;23(3):e14060. doi: 10.1111/acel.14060

FIGURE 4.

FIGURE 4

Fisetin improves endothelial function by ameliorating whole‐cell and mitochondrial oxidative stress. Whole‐cell aortic reactive oxygen species (ROS) levels (n = 6–8) (a). Aortic protein abundance of NADPH oxidase (n = 8) (b) and CuZn superoxide dismutase (SOD; n = 11–12) (c) with representative virtual blot bands, right. Endothelium‐dependent dilation (EDD) in isolated carotid arteries in response to acetylcholine (ACh) in the presence or absence of the SOD mimetic, TEMPOL (1 mM, 60 min preincubation; n = 7–8) (d). Aortic mitochondrial ROS levels (n = 6–10) (e). Aortic protein abundance of phosphorylated p66SHC (p‐p66SHC; n = 11–12) (f) and MnSOD (n = 11–12) (g) with representative virtual blot bands, right. EDD in carotid arteries in response to ACh in the presence or absence of the mitochondrial‐specific antioxidant, MitoQ (1 μM; 60 min preincubation; n = 5–7) (h). Values represent mean ± SEM. *p < 0.05 old vehicle versus old fisetin; ^p < 0.05 versus ACh alone.