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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Aldose reductase mediates endothelial cell dysfunction induced by high uric acid concentrations

Fig. 1

Effect of different UA concentration on intracellular oxidative stress, NO release and AR activity. Endothelial cells were cultured in the presence of 300, 600 μM UA or without UA for 24 h. a Total ROS was reduced in cells treated with 300 μM UA (# P < 0.05 vs. control, n = 3), but increased in cells treated with 600 μM UA (*P < 0.05 vs. control, n = 3). b Compared to the control, the NO level was not significantly different in the 300 μM UA-treated group, but was reduced in the 600 μM UA-treated group (*P < 0.05 vs. control, n = 6). c Cells were treated with 600 μM UA at 6, 12, 24, and 48 h; total ROS production increased (*P < 0.05 vs. control, n = 6), ROS production was saturated at 24–48 h (#P < 0.05 vs. 6 h or 12 h, n = 6), and (d) NO levels decreased at 6 h (*P < 0.05 vs. control, n = 6). e AR expression increase at 24 h (*P < 0.05 vs. control, n = 3) in the high concentration of uric acid. There is no significate change at the 6 h or 12 h. f, g After intraperitoneal injection with oxonic acid potassium salt and UA for 10 days, serum UA levels in wild-type C57BL/6 mice increased significantly (*P < 0.05 vs. control, n = 6), whereas serum NO levels declined (*P < 0.05 vs. control, n = 6). g AR activity increased in endothelial cells cultured in the presence of 600 μM UA for 24 h, but there was no change upon treatment with 300 μM UA (*P < 0.05 vs. control, n = 6)

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