title: Modulation of phase II enzymes by sulforaphane: implications for its cardioprotective potential.
abstract: Oxidative stress plays a major role in the pathophysiology of cardiac disorders, but the experimental data on the protective effects of exogenous antioxidants are controversial. A promising cardioprotective strategy may be through the induction of the endogenous antioxidants and phase II enzymes by chemical inducers. Sulforaphane is an isothiocyanate derived from cruciferous vegetables, and it has gained attention mainly as a potential chemopreventive agent in part through the induction of detoxifying enzymes. Accordingly, this study was undertaken to investigate the time-dependent induction of gene transcription, protein expression, and enzyme activity of antioxidant and phase II enzymes [glutathione reductase, glutathione-S-transferase, glutathione peroxidase, NAD(P)H:quinone oxidoreductase-1, thioredoxin reductase] by sulforaphane in cultured rat neonatal cardiomyocytes. The potential cardioprotective action of sulforaphane was confirmed by the decrease in intracellular reactive oxygen species production, the increase in cell viability, and the decrease in DNA fragmentation after long-term treatment accompanied by the induction of antioxidants and phase II enzymes in cardiomyocytes.
authors.affiliation: Department of Biochemistry G Moruzzi, University of Bologna, Bologna, Italy.
authors.forename: Cristina
authors.initials: C
authors.lastname: Angeloni
authors.forename: Emanuela
authors.initials: E
authors.lastname: Leoncini
authors.forename: Marco
authors.initials: M
authors.lastname: Malaguti
authors.forename: Sabrina
authors.initials: S
authors.lastname: Angelini
authors.forename: Patrizia
authors.initials: P
authors.lastname: Hrelia
authors.forename: Silvana
authors.initials: S
authors.lastname: Hrelia
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004789:Enzyme Activation / Q000187:drug effects; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D005980:Glutathione Reductase / Q000235:genetics / Q000378:metabolism; D005982:Glutathione Transferase / Q000235:genetics / Q000378:metabolism; D006801:Humans; D017879:Isothiocyanates; D050217:Metabolic Detoxication, Phase II; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology; D018384:Oxidative Stress; D011808:Quinone Reductases / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013454:Sulfoxides; D013861:Thiocyanates / Q000494:pharmacology*
chemical_list: D002316:Cardiotonic Agents; D017879:Isothiocyanates; D017382:Reactive Oxygen Species; D013454:Sulfoxides; D013861:Thiocyanates; D005979:Glutathione Peroxidase; D011808:Quinone Reductases; D005980:Glutathione Reductase; D005982:Glutathione Transferase; C016766:sulforaphane