Epidemiological evidence indicates several health benefits of the consumption of broccoli, especially related to
chemoprevention. Because broccoli contains high amounts of
selenium and
glucosinolates (particularly
glucoraphanin and
isothiocyanate sulforaphane), which can produce redox-regulated cardioprotective
protein thioredoxin (Trx), it was reasoned that consumption of broccoli could be beneficial to the heart. To test this hypothesis, a group of rats were fed broccoli (slurry made with water) through gavaging; control animals were gavaged water only. After 30 days, the rats were sacrificed; isolated hearts perfused via working mode were made ischemic for 30 min followed by 2 h of reperfusion. The results demonstrated significant cardioprotection with broccoli as evidenced by improved postischemic ventricular function, reduced
myocardial infarct size, and decreased cardiomyocyte apoptosis accompanied by reduced
cytochrome c release and increased
pro-caspase 3 activities.
Ischemia/reperfusion reduced both
RNA transcripts and
protein levels of the
thioredoxin superfamily including Trx1, Trx2,
glutaredoxin Grx1, Grx2, and
peroxiredoxin (Prdx), which were either restored or enhanced with broccoli. Broccoli enhanced the expression of Nrf2, a cytosolic suppressor of Keap1, suggesting a role of antioxidant response element (ARE) in the induction of Trx. Additionally, broccoli induced the expression of another cardioprotective
protein, heme oxygenase (HO)-1, which could be transactivated during the activation of Trx. Examination of the survival signal revealed that broccoli caused the phosphorylation of Akt and the induction of Bcl2 in concert with the activation of redox-sensitive
transcription factor NF kappa B and
Src kinase, indicating a role of Akt, Bcl2, and cSrc in the generation of survival signal. Taken together, the results of the present study indicate that the consumption of broccoli triggers cardioprotection by generating a survival signal through the activation of several survival
proteins and by redox cycling of
thioredoxins.