Background and Objective; Oxidative stress has been implicated in the pathogenesis of a variety of cardiovascular disease including ischemic heart disease and its related heart failure. Peroxisome proliferator-activated receptors gamma (PPAR款) agonist had been shown insulin sensitivity improvement, anti-inflammation and anti-apoptosis. There are scarce data about the relationship between PPAR款 agonist, Rosiglitazone (RSG) and Thioredoxin (TRx) system in oxidative stressed cardiomyocyte (CMC). We will try to provide evidences that PPAR款 agonist protects CMCs from H₂O₂-induced apoptosis through up-regulation of TRx expression. Methods; Neonatal rat cardiomyocytes (rCMCs) from the ventricles of 1-day-old Sprague-Dawley rats were primary cultured. 1uM RSG or media as control was pretreated to rCMCs (3X10⁵ cells) before the oxidative stress. Oxidative stress was induced by 0.5 mM of H₂O₂ for 4 hours in 2 groups. Proportion of apoptosis was measured by FACS analysis with Annexin-V-PE staining. TRx system component, e.g. TRx, TRx interacting protein (TxNip) and TRx reductase (TRxR) and cell survival pathway (p-Akt /Akt, Bcl-2/Bax) were measured by Western blot analysis. Results; RSG effectively reduced H₂O₂ related rCMCs apoptosis compared to H₂O₂ control (10.99% vs 27.06%, difference 146%). Also, the expressions of TRx, p-Akt /Akt, Bcl-2/Bax were significantly increased in RSG group. However Txnip and TrxR expression was comparable between two groups.Conclusion; RSG effectively protects rCMCs from apoptosis related with H₂O₂ induced oxidative stress. This phenomenon is closely related with RSG inducing TRx overexpression.