Urotensin II-induced insulin resistance is mediated by NADPH oxidase-derived reactive oxygen species in HepG2 cells

Figure 4 Urotensin II elevates reactive oxygen species production and NADPH oxidase subunit expression. HepG2 cells were cultured with 0, 1, 10, or 100 nmol/L urotensin II (UII) for 24 h, with or without prior stimulation with apocynin (200 μmol/L, 30 min). Intracellular reactive oxygen species (ROS) production was elevated in a dose- and time-dependent manner (A, B). NADPH oxidase subunits gp91^phox, p67^phox, p47^phox, and p40^phox were significantly increased in response to UII (100 nmol/L, 24 h) (C). Apocynin pretreatment inhibited ROS generation (D). Data from at least three independent experiments are presented as the mean ± SD. ^aP < 0.05, ^bP < 0.01 vs control group; ^gP < 0.05 vs UII treatment alone.