Comparison of the protective effects of steamed and cooked broccolis on ischaemia-reperfusion-induced cardiac injury.
Recently, broccoli, a vegetable of the Brassica family, has been found to protect the myocardium from ischaemic reperfusion injury through the redox signalling of sulphoraphane, which is being formed from glucosinolate present in this vegetable. Since cooked broccoli loses most of its glucosinolate, we assumed that fresh broccoli could be a superior cardioprotective agent compared to cooked broccoli. To test this, two groups of rats were fed with fresh (steamed) broccoli or cooked broccoli for 30 d, while a third group was given vehicle only for the same period of time. After 30 d, all the rats were sacrificed, and the isolated working hearts were subjected to 30 min ischaemia followed by 2 h of reperfusion. Both cooked and steamed broccolis displayed significantly improved post-ischaemic ventricular function and reduced myocardial infarction and cardiomyocyte apoptosis compared to control, but steamed broccoli showed superior cardioprotective abilities compared with the cooked broccoli. Corroborating with these results, both cooked and steamed broccolis demonstrated significantly enhanced induction of the survival signalling proteins including Bcl2, Akt, extracellular signal-regulated kinase 1/2, haemoxygenase-1, NFE2 related factor 2, superoxide dismutase (SOD1) and SOD2 and down-regulation of the proteins (e.g. Bax, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase) of the death signalling pathway, steamed broccoli displaying superior results over its cooked counterpart. The expressions of proteins of the thioredoxin (Trx) superfamily including Trx1 and its precursor sulphoraphane, Trx2 and Trx reductase, were enhanced only in the steamed broccoli group. The results of the present study documented superior cardioprotective properties of the steamed broccoli over cooked broccoli because of the ability of fresh broccoli to perform redox signalling of Trx.
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA.
Subhendu
S
Mukherjee
Istvan
I
Lekli
Diptarka
D
Ray
Hiranmoy
H
Gangopadhyay
Utpal
U
Raychaudhuri
Dipak K
DK
Das
D000818:Animals; D017209:Apoptosis; D001937:Brassica / Q000737:chemistry*; D006358:Hot Temperature; D017879:Isothiocyanates; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009203:Myocardial Infarction / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000166:cytology; D010084:Oxidation-Reduction; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D013454:Sulfoxides; D013861:Thiocyanates / Q000032:analysis; D013880:Thioredoxin-Disulfide Reductase / Q000032:analysis; D013879:Thioredoxins / Q000032:analysis; D016277:Ventricular Function, Left
D017879:Isothiocyanates; D013454:Sulfoxides; D013861:Thiocyanates; C495697:Txn1 protein, rat; C516113:Txn2 protein, rat; D013879:Thioredoxins; D013880:Thioredoxin-Disulfide Reductase; D020928:Mitogen-Activated Protein Kinases; C016766:sulforaphane