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. 2021 Aug 18;46:102108. doi: 10.1016/j.redox.2021.102108

Fig. 3.

Fig. 3

NOX/ROS pathway is crucial in the excess UA-induced deregulation of ADMA−DDAH-2 system and EC dysfunction. HAECs were treated with 12 mg/dL uric acid (UA) for indicated time period (min). (A) The changes in NADP+/NADPH ratio was examined using the NADP+/NADPH assay kit. The fold induction is defined as the ratio of NADP+/NADPH at the indicated times relative to that the time zero group set as 1. (B and C) Intracellular levels of superoxide and hydrogen peroxide were evaluated. (D–F) HAECs were pretreated with the ROS scavenger NAC (10 mM) or the NADPH oxidase inhibitor apocynin (150 μM) for 2 h and subsequently treated with 12 mg/dL UA for 24 h. (D) Intracellular ADMA was assessed using a commercial assay kit. (E) NO production was assessed using Griess's assay. (F) Monocyte–EC adhesion assay was conducted by performing fluorometry and photomicrography. Data are expressed as means ± SEMs from five independent experiments. *Statistically significant difference (P < 0.05) relative to vehicle group; #Statistically significant difference (P < 0.05) relative to UA-treated group.