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. 2018 Feb 28;2018:1047810. doi: 10.1155/2018/1047810

Figure 3.

Figure 3

DMY increases NO generation and decreases intracellular and extracellular ADMA concentration in a miR-21-dependent manner in TNF-α treated HUVECs. (a) DMY increases eNOS (ser1177) phosphorylation in a miR-21-dependent manner; (b) DMY increases NO concentration in cell medium induced by TNF-α in a miR-21-dependent manner; (c) DMY decreases intracellular ADMA concentration induced by TNF-α in a miR-21-dependent manner; (d) DMY decreases extracellular ADMA concentration induced by TNF-α in a miR-21-dependent manner. Data was expressed as mean ± SD, n = 3, ∗P < 0.05 versus control, ∗∗P < 0.05 versus control, #P < 0.05 versus TNF-α, ##P < 0.05 versus control, +P < 0.05 versus TNF-α + DMY (25 μM), and ++P < 0.01 versus TNF-α + DMY (25 μM). ∗∗P < 0.01 versus agomir NC, $$P < 0.01 versus antagomir NC, ##P < 0.01 versus TNF-α + miR-21 agomir NC, and ΦΦP < 0.01 versus TNF-α + miR-21 antagomir NC in (a).