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During reperfusion phase, SFN curtailed further myocardial damage and this helped in reducing infarct size more effectively than the conventional mechanical maneuver of post-conditioning (PostC), which made the authors propose that the transient elevation of Nrf2 activation with upregulation of both phase I and II enzymes serves as a long-term cardioprotective mechanism against experimental myocardial ischemia/reperfusion injury in Wistar rats [62]
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