Fig. 6.

Aminoguanidine (AG) protects against glyoxal-induced inhibition of [³H]-thymidine incorporation by endothelial cells. BPAECs (90% confluent), grown in 35-mm dishes (6-well culture plate) were treated for 12 h with MEM alone or MEM-containing a glyoxal (1, 5, and 10 mM) or b cells were pre-treated with AG HCl (1 mM) or AG nitrate (1 mM) for 1 h and then treated with MEM alone, MEM-containing AG HCl or AG nitrate (1 mM), MEM-containing glyoxal (1 mM), or MEM-containing AG HCl or AG nitrate (1 mM) + glyoxal (1 mM) for 12 h at 37°C in a humidified environment of 5% CO₂–95% air. At the end of incubation, cells were labeled with [³H]-thymidine (1 µCi/ml) in complete EC medium for 24 h. Cell replication at the end of the treatment was assayed by determining [³H]-thymidine incorporation into the cells as outlined in the Materials and methods section. Data represent means ± SD of three independent experiments. * Significantly different at P < 0.05 as compared to the cells treated with MEM alone. ** Significantly different at P < 0.05 as compared to the control cells treated with MEM-containing glyoxal