EC Number   |
Activating Compound |
Reference |
|---|
   1.6.3.1 | (+)-(S)-2-(6-methoxynaphthalen-2-yl)propanoic acid |
i.e. naproxen, nonsteroidal anti-inflammatory drug. Marked increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin |
688605 |
| 1.6.3.1 | (+)-(S)-2-(6-methoxynaphthalen-2-yl)propanoic acid |
i.e. naproxen, nonsteroidal anti-inflammatory drug. Treatment increases isoform Nox2 expression in endothelial cells and diminishes production of bioactive nitric oxide. In healthy volunteers, treatment reduces nitroglycerin-induced, nitric oxide-mediated vasodilatation of the brachial artery |
688605 |
| 1.6.3.1 | 11alpha,9alpha-epoxymethanoprostaglandin F 2alpha |
induces the expression of subunits p22phox and gp91phox |
688597 |
| 1.6.3.1 | 2,4,6-trinitrophenyl-bovine serum albumin |
induces reactive oxygen species generation, which occurrs immediately. 2,4,6-Trinitrophenyl-bovine serum albumin but not TG causes extracellular release of superoxide anion/hydrogen peroxide, which is blocked by diphenyleneiodonium, apocynin, and wortmannin. When used together, 2,4,6-trinitrophenyl-bovine serum albumin and thapsigargin evoke the release of leukotriene C4, tumor necrosis factor-alpha, and interleukin-13 as well as reactive oxygen species generation synergistically |
685384 |
| 1.6.3.1 | 2,6-dichlorophenolindophenol |
- |
636496 |
| 1.6.3.1 | 2-(2-(2,6-dichlorophenylamino)-phenyl)acetic acid |
i.e. diclofenac, nonsteroidal anti-inflammatory drug. Marked increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin |
688605 |
| 1.6.3.1 | 2-(2-(2,6-dichlorophenylamino)-phenyl)acetic acid |
i.e. diclofenac, nonsteroidal anti-inflammatory drug. Treatment increases isoform Nox2 expression in endothelial cells and diminishes production of bioactive nitric oxide. In healthy volunteers, treatment reduces nitroglycerin-induced, nitric oxide-mediated vasodilatation of the brachial artery |
688605 |
| 1.6.3.1 | 4-(4-methylsulfonylphenyl)-3-phenyl-5H-furan-2-one |
i.e. rofecoxib, nonsteroidal anti-inflammatory drug. Moderate increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin |
688605 |
| 1.6.3.1 | 4-(4-methylsulfonylphenyl)-3-phenyl-5H-furan-2-one |
i.e. rofecoxib, nonsteroidal anti-inflammatory drug. Treatment increases isoform Nox2 expression in endothelial cells and diminishes production of bioactive nitric oxide. In healthy volunteers, treatment reduces nitroglycerin-induced, nitric oxide-mediated vasodilatation of the brachial artery |
688605 |
| 1.6.3.1 | 4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide |
i.e. celecoxib, nonsteroidal anti-inflammatory drug. Moderate increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin |
688605 |
