Fig 1: Involvement of the Thioredoxin System in the mode of action of KH176(m). (a) KH176 and KH176m can rescue P4 cells from BSO (200 µM)-induced death, their efficiency depends on an active Thioredoxin System since the presence of 100 nM AFN inhibits the rescue. ***p < 0.001 as compared to the indicated control. Increasing amounts of KH176 (b) or KH176m (c) rescue BSO (200 uM) treated cells, different concentrations of AFN affect the efficacy, but not potency of KH176(m). (d) the antioxidant activity of KH176(m) is not affected by inhibition of the Thioredoxin System by AFN (100 nM). ***p < 0.001 and n.s. = non-significant both as compared to the indicated bars. (e) KH176m but not KH176 enhances the Thioredoxin System/Peroxiredoxin-dependent consumption of NADPH. TrxR1, Trx1 and Prdx2 were incubated with NADPH and H2O2 in the presence or absence of 100 µM of KH176 or KH176m. The graph reports the fluorescence signal of NADPH over time. - = no KH compounds. For all panels: unless otherwise indicated the data points represent the average of triplicate measurements and are normalized on the untreated condition, SD is indicated. ***p < 0.001, n.s. = non-significant.
Supplier Page from Novus Biologicals, a Bio-Techne Brand for Recombinant Human Thioredoxin Reductase 1/TRXR1 His Protein