Activating Compound | Comment | Organism | Structure |
---|---|---|---|
(+)-(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 | Rattus norvegicus | |
(+)-(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 | Homo sapiens | |
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 | Rattus norvegicus | |
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 | Homo sapiens | |
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 | Rattus norvegicus | |
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 | Homo sapiens | |
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 | Rattus norvegicus | |
4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide | i.e. celecoxib, 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 | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Rattus norvegicus | - |
spontaneously hypertensive rats | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
endothelium | - |
Homo sapiens | - |