Fig. 3.

Nox2 inhibitors attenuate TNFα-induced mitogen-activated protein kinase (MAPK) activation in HAECs. (A) Representative Western blots (left) and cumulative data (right) showing concentration dependent inhibition by CPP11G and CPP11H of TNFα (10 ng/ml, 10 min)-stimulated p38 MAPK activation. The densities of phospho-p38 were normalized to the levels of total p38 detected in the same samples, n = 6–8. (****p < 0.0001 vs. unstimulated, #p < 0.05 vs. TNFα, ##p < 0.01 vs. TNFα, ####p < 0.0001 vs. TNFα). (B) Representative Western blots (left) and cumulative data (right) showing concentration dependent inhibition by CPP11G and CPP11H of TNFα (10 ng/ml, 20 min)-stimulated JNK phosphorylation. The densities of phospho-JNK were normalized to the levels of total JNK detected in the same samples, n = 7. (****p < 0.0001 vs. unstimulated, #p < 0.05 vs. TNFα, ##p < 0.01 vs. TNFα). (C) Representative Western blots (left) and cumulative data (right) showing concentration dependent attenuation by CPP11G and CPP11H of TNFα (10 ng/ml, 1h)-stimulated cJun phosphorylation. The densities of phospho-cJun were normalized to the levels of total cJun detected in the same samples, n = 6. (****p < 0.0001 vs. unstimulated, #p < 0.05 vs. TNFα, ####p < 0.0001 vs. TNFα). (D) Representative Western blots (left) and cumulative data (right) showing the effects of CPP11G (10 μmol/l) and CPP11H (10 μmol/l) on TNFα (10 ng/mL, 1h)-modified phospho-cJun levels on the nuclear fraction. The densities of phospho-cJun were normalized to the levels of histone detected in the same samples, n = 3. (***p < 0.001 vs. control, ###p < 0.001 vs. TNFα).