title: Protective effects of EGCg or GCg, a green tea catechin epimer, against postischemic myocardial dysfunction in guinea-pig hearts.
abstract: The protective effects of (-)-epigallocatechin-3-gallate (EGCg) or the C-2 epimer, (-)-gallocatechin-3-gallate (GCg), afforded by their antioxidative activity among green tea catechins were investigated in perfused guinea-pig Langendorff hearts subjected to ischemia and reperfusion. The recovery (%) of the left ventricular developed pressure from ischemia by reperfusion was 34.4% in the control, while in the presence of EGCg (3x10(-5) M) or GCg (3x10(-6) M, a more diluted concentration than that of EGCg), it led to a maximal increase of 78.4% or 76.2%, consistent with a significant preservative effect on the tissue level of ATP at the end of ischemia or reperfusion. In the perfused preparation of mitochondria, EGCg (10(-5) M) inhibited mitochondrial Ca(2+) elevation by changes in the Ca(2+) content or the acidification of perfusate, similarly to findings with cyclosporin A, a well known inhibitor of the mitochondrial permeability transition pore. By in vitro electron paramagnetic resonance (EPR), EGCg or GCg was found to directly quench the activity of active oxygen radicals, with the strongest activity in tea catechins. EGCg or GCg decreased the caspase-3 activity induced apoptosis. Therefore, it is concluded that the beneficial effects of EGCg or GCg play an important role in ischemia-reperfusion hearts in close relation with nitric oxide (NO), active oxygen radicals and biological redox systems in mitochondria.
authors.affiliation: Department of Cardiac Surgery, Aichi Medical University School of Medicine, Aichi, Japan.
authors.forename: Masaya
authors.initials: M
authors.lastname: Hirai
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Hotta
authors.forename: Naohisa
authors.initials: N
authors.lastname: Ishikawa
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Wakida
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Fukuzawa
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Isobe
authors.forename: Akinobu
authors.initials: A
authors.lastname: Nakano
authors.forename: Taku
authors.initials: T
authors.lastname: Chiba
authors.forename: Norihisa
authors.initials: N
authors.lastname: Kawamura
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D004195:Disease Models, Animal; D004578:Electron Spin Resonance Spectroscopy; D005260:Female; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010477:Perfusion / Q000379:methods; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; C417940:gallocatechin gallate; D002392:Catechin; C045651:epigallocatechin gallate; D053148:Caspase 3; D002118:Calcium