Key result
Recombinant human thioredoxin (2 mg/kg) significantly decreased myocardial apoptosis and reduced infarct size in mice following ischemia and reperfusion (P<0.01).
Why the study?
Does recombinant human Thioredoxin reduce myocardial apoptosis and infarct size in a mouse model of ischemia/reperfusion injury?
Population
Mice subjected to 30 minutes of myocardial ischemia and reperfusion, and cultured adult cardiomyocytes
Comparison
Recombinant human Thioredoxin 0.7-20 mg kg i.p… vs Untreated/vehicle control (implied)
Design
Preclinical
Authors
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May support thioredoxin as cardioprotective in ischemia/reperfusion; leaves open translation to human therapy.
Does recombinant human Thioredoxin reduce myocardial apoptosis and infarct size in a mouse model of ischemia/reperfusion injury?
p-value: p=<0.01
Recombinant human thioredoxin reduces myocardial apoptosis and infarct size following ischemia/reperfusion injury by decreasing oxidative and nitrative stress in a preclinical model.
Tao et al. (2006) studied Myocardial ischemia/reperfusion injury. Recombinant human Thioredoxin (rhTrx) was evaluated on Myocardial apoptosis and infarct size (p=<0.01). Recombinant human thioredoxin (2 mg/kg) significantly decreased myocardial apoptosis and reduced infarct size in mice following ischemia and reperfusion (P<0.01).
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