Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway

Figure 4

DMY increases DDAH1 expression and enhances DDAH metabolizing activity in a miR-21-dependent manner in TNF-α treated HUVECs. (a) Blockade of miR-21 expression increases DDAH1 protein expression induced by TNF-α; (b) DMY increases DDAH1 protein expression induced by TNF-α in a miR-21-dependent manner; (c) DMY increases DDAH1 mRNA expression induced by TNF-α in a miR-21-dependent manner; (d) DMY increases DDAH metabolic activity induced by TNF-α in a miR-21-dependent manner; (e) both TNF-α and DMY have no effect on DDAH2 mRNA expression. Data was expressed as mean ± SD, , versus control, versus control, versus TNF-α, versus TNF-α, versus TNF-α + DMY (25 μM), and versus TNF-α + DMY (25 μM).

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