Cur inhibited TGF‐β1‐induced EndMT by stimulating NRF‐2 and DDAH to degrade ADMA. A, After treatment with different concentrations (0, 0.5, 1, 2.5, 5, 10, or 20 μmol/L) of ML385 (NRF‐2 inhibitor; SML1833; Sigma), the cell proliferation was detected at 0, 24, 48 and 72 h. HUVECs were treated with TGF‐β1 (10 µg/L), TGF‐β1 (10 µg/L) + 2.5 μmol/L ML385, TGF‐β1 (10 µg/L) + 2.5 μmol/L ML385 + 5 μmol/L Cur, and TGF‐β1 (10 µg/L) + 2.5 μmol/L ML385 + 10 μmol/L Cur for 48 h. B, NRF‐2 mRNA expression was detected. C, Protein levels of VE‐cadherin, vimentin, DDAH and NRF‐2 were detected. D, E, Immunofluorescence detection of CD31 (D) and α‐SMA (E) at a magnification of 200×. *P < .05, **P < .01, and ***P < .001 vs 0 μmol/L ML385 or TGF‐β1; ##
P < .01 and ###
P < .001 vs TGF‐β1 + ML385. (A) , 0 μmol/L ML385; , 0.5 μmol/L ML385; , 1 μmol/L ML385; , 2.5 μmol/L ML385; , 5 μmol/L ML385; , 10 μmol/L ML385; , 20 μmol/L ML385; , TGF‐β1; , TGF‐β1 + ML385; , TGF‐β1 + ML385 + 5 μmol/L Cur; , TGF‐β1 + ML385 + 10 μmol/L Cur