Thioredoxin reduces post‐ischemic myocardial apoptosis by reducing oxidative/nitrative stress

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Abstract
Background and purpose: Thioredoxin (Trx) is an oxidoreductase that prevents free radical‐induced cell death in cultured cells. Here we assessed the mechanism(s) underlying the cardioprotective effects of Trxin vivo.Experimental approach: The effects of myocardial ischemia (30 min) and reperfusion were measured in mice, with assays of myocardial apoptosis, superoxide production, NOx and nitrotyrosine content, and myocardial infarct size. Recombinant human Trx (rhTrx, 0.7–20 mg kg‐1, i.p.) was given 10 min before reperfusion.Key results: Treatment with 2 mg kg‐1rhTrx significantly decreased myocardial apoptosis and reduced infarct size (PPμMfor 3 h) resulting in a nitrotyrosine content comparable to that seen in the ischemic/reperfused heart and causing significant cardiomyocyte apoptosis (PPBritish Journal of Pharmacology(2006)149, 311–318. doi:10.1038/sj.bjp.0706853