Hydrogen sulfide provides cardioprotection against @entity741 reperfusion @entity130 in the XXXX state through the activation of the RISK pathway.

@entity1 @entity17122 @entity296 @entity6 @entity8837 @entity19 @entity1188 @entity741 @entity453 @entity204 @entity130
BACKGROUND: @entity453 remains the principal cause of @entity204 in @entity1 with @entity6 . @entity6 @entity19 display exacerbated @entity130 following @entity741 -reperfusion (MI/R) and are resistant to most therapeutic interventions. We have reported that @entity17122 ( @entity17122 ) therapy confers cardioprotection during MI/R in non- @entity6 @entity19 . Here we tested the hypothesis that @entity17122 therapy would limit the extent of @entity296 following MI/R when administered at the time of reperfusion. METHODS AND RESULTS: @entity6 @entity19 (db/db, 12  weeks of age) were subjected to transient @entity741 for a period of 30  minutes followed by reperfusion up to 24  hours. @entity17122 (0.05 to 1  mg/kg) or saline (vehicle) was administered into the left ventricular lumen at the time of reperfusion. @entity17122 therapy significantly decreased @entity296 in the db/db @entity6 @entity19 , as evidenced by a reduction in @entity1188 size and circulating troponin-I levels. The reduction in @entity296 was also associated with a reduction in oxidative stress and a decrease in cleaved caspase-3 expression. In an effort to evaluate the signaling mechanism responsible for the observed cardioprotection, additional groups of @entity19 were sacrificed during early reperfusion. Hearts were excised and processed for Western blot analysis. These studies revealed that @entity17122 therapy activated the @entity8837 arm of the Reperfusion Injury Salvage Kinase (RISK) pathway. CONCLUSION: These findings provide important information that myocardial @entity8837 activation by @entity17122 therapy following MI/R sets into motion events, which ultimately lead to cardioprotection in the setting of @entity6 .
