Abbreviations DCIP 2,6-dichloroindophenol GCL glutamate cysteine ligase GSH reduced glutathione GSSG oxidized glutathione IR ischemia-reperfusion LDH lactate dehydrogenase PMSF phenylmethylsulphonyl fluoride QR quinone reductase TBARS thiobarbituric acid reactive substances
Introduction
In ischemia-reperfusion, disturbances in cellular homeostasis threaten the life of myocardial cells. Although, recent notions have implicated myocardial cell renewal to be of possible clinical importance after myocardial infarction [1, 2], cardiac tissue has limited ability to replace dead cells [3] and therefore prevention of cell death during ischemiareperfusion bears therapeutic implications.
As generation of reactive oxygen species is a primary cause of ischemia-reperfusion injury [4], one of the preventive strategies is to reduce the magnitude of oxidative stress. Reduction of oxidative stress can be achieved through administration of exogenous antioxidants, although administration of individual antioxidant vitamins has not always produced favorable results [5]. An alternative strategy is to stimulate production of endogenous antioxidants [6, 7]. Phase 2 detoxification enzymes are an important group of endogenous enzymes under control of the Nrf2/antioxidant response element (ARE) pathway that provide defense against oxidative stress and xenobiotics [8].
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