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myocardial ischemia\/reperfusion (MI\/R) injury. Activation of silent information regulator 1 (SIRT1) signaling attenuates MI\/R injury by reducing oxidative damage and inflammation response. This study investigated the antioxidative  and anti\u2010inflammatory effects of BBR treatment in MI\/R condition and elucidated its potential mechanisms. Sprague\u2010Dawley rats were treated with BBR in the absence or presence of the SIRT1 inhibitor sirtinol (Stnl) and then subjected to MI\/R injury. BBR conferred cardioprotective effects by improving postischemic cardiac function, decreasing infarct size, reducing apoptotic index, diminishing serum creatine kinase and lactate dehydrogenase levels, upregulating  SIRT1, Bcl\u20102 expressions,  and downregulating  Bax and caspase\u20103 expressions. Stnl attenuated these effects by inhibiting SIRT1 signaling. BBR treatment also reduced myocardium superoxide generation, gp91<jats:sup>phox<\/jats:sup> expression, malondialdehyde (MDA) level, and cardiac inflammatory markers and increased myocardium superoxide dismutase (SOD) level. However, these effects were also inhibited by Stnl. Consistently, BBR conferred similar antioxidative  and anti\u2010inflammatory effects against simulated ischemia reperfusion injury in cultured H9C2 cardiomyocytes. SIRT1 siRNA administration also abolished these effects. In summary, our results demonstrate that BBR significantly improves post\u2010MI\/R cardiac function recovery and reduces infarct size against MI\/R injury possibly due to its strong antioxidative  and anti\u2010inflammatory activity. 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