INTRODUCCIÓN: REVISIÓN CRITICA DEL PROBLEMA

CAPÍTULO IX
with HSA or gHSA (2.16 ± 0.32 NOX4 fold change for HSA+SP600125, p < 0.05, n
= 6; Figure 1a; 1.25 ± 0.10 NOX4 fold change for gHSA vs. 2.39 ± 0.51 NOX4 fold
change for gHSA+SP600125, p < 0.05, n = 6; Figure 1a). Also, the presence of
AP-1 inhibitor increased significantly P22PHOX expression in the presence of
HSA (1.14 ± 0.07 P22PHOX fold change forHSA+SP600125, p < 0.05, n = 5;
Figure 1b) but SP600125 in combination with gHSA did not modify P22PHOX
expression with respect to gHSA alone (1.12 ± 0.06 22PHOX fold change for
gHSA vs. 1.12 ± 0.07 P22PHOX fold change for gHSA+SP600125, p > 0.05, n =
5; Figure 1b).
These results indicated the involvement of NF-κB in the gHSA-induced NOX4
expression. However, SP600125 modified NOX4 expression independently of
HSA or gHSA. With regard to P22PHOX, AP-1 inhibition in the presence of HSA
significantly up-regulated P22PHOX expression to the same levels than gHSA
treatments.
Activation of NF-κB by gHSA
Since BAY 11-7082 2μM reverted gHSA-induced NOX4 up-regulation, we studied
the effects of gHSA 25μg/mL for 4 hours in NF-κB activation. We carried out
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