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Literature summary for 1.6.3.1 extracted from

  • Qin, F.; Simeone, M.; Patel, R.
    Inhibition of NADPH oxidase reduces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction (2007), Free Radic. Biol. Med., 43, 271-281.
    View publication on PubMed

Application

Application Comment Organism
medicine in rabbits with heart failure induced by myocardial infarction, treatment with inhibitor apocynin reduces NADPH oxidase activity, subunit p47phox protein, oxidative stress, myocyte apoptosis, and Bax protein, increases Bcl-2 protein, and ameliorates left ventricular dilatation and dysfunction Oryctolagus cuniculus

Inhibitors

Inhibitors Comment Organism Structure
apocynin in rabbits with heart failure induced by myocardial infarction, apocynin reduces NADPH oxidase activity, subunit p47phox protein, oxidative stress, myocyte apoptosis, and Bax protein, increases Bcl-2 protein, and ameliorates left ventricular dilatation and dysfunction Oryctolagus cuniculus

Organism

Organism UniProt Comment Textmining
Oryctolagus cuniculus
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Source Tissue

Source Tissue Comment Organism Textmining
heart rabbits with heart failure induced by myocardial infarction exhibit left ventricular dilatation and systolic dysfunction. Changes are associated with increases in NADPH oxidase activity, subunit p47phox protein expression, 8-hydroxydeoxyguanosine expression, 4-hydroxy-2-nonenal expression, myocyte apoptosis, and Bax protein and a decrease in Bcl-2 protein Oryctolagus cuniculus
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