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. 2020 Apr 17;24(10):5911–5925. doi: 10.1111/jcmm.15278

FIGURE 5.

FIGURE 5

Overexpression of miR‐21 inhibits nitric oxide (NO) production and abrogates dihydromyricetin (DMY)‐attenuated EC activation in response to ox‐LDL. HUVECs were transfected with 100 nm agomir NC or miR‐21 agomir for 24 h and then treated with ox‐LDL (120 μg/mL) or ox‐LDL plus DMY (25 μmol/L) for 16 h and harvested for indicated experiments. A and B, ELISA analysis of NO levels in supernatant (A) and cell lysates (B). n = 3 independent experiments. C, Fluorescent NO probe analysis of NO levels in live HUVECs. Scale: 50 μm. n = 3 independent experiments. D, Western blot analysis of VCAM‐1 expression. n = 3 independent experiments. E, Real‐time qPCR analysis of VCAM‐1. Expression of VCAM‐1 was normalized to GAPDH. n = 3 independent experiments. F, Representative images and quantification show THP‐1 cells adhering to HUVECs after treatment. Scale: 100 μm. n = 3 independent experiments. G, Real‐time qPCR analysis of miR‐21. Expression of miR‐21 was normalized to U6. n = 3 independent experiments. Data shown are mean ± SEM. *P < .05