Fig. 6.
Contributions of Akt, extracellular signal-related kinase (ERK)1/2, and p38 mitogen-activated protein kinase (MAPK) to the CO inhibition of NADPH oxidase activity. Fractionated confluent quiescent CMVEC, untreated or pretreated with triciribine (TCN; Akt inhibitor, 1 μM), PD98059 (ERK1/2 inhibitor, 20 μM), and SB203580 (p38 MAPK inhibitor, 5 μM) were exposed to TNF-α (15 ng/ml, 1 h). NADPH oxidase activity was determined as O2·− production from NADPH (100 μM), normalized to the protein amount, and expressed as percentage of the baseline control. Values are means ± SE. *P < 0.05 compared with the baseline activity. †P < 0.05 compared with TNF-α alone.