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Ischemic postconditioning confers cardioprotection and prevents reduction of Trx-1 in young mice, but not in middle-aged and old mice.
Perez, Virginia; D Annunzio, Verónica; Mazo, Tamara; Marchini, Timoteo; Caceres, Lourdes; Evelson, Pablo; Gelpi, Ricardo J.
Afiliação
  • Perez V; Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires, JE Uriburu 950 - 2nd floor, 1114, Buenos Aires, Argentina.
  • D Annunzio V; Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires, JE Uriburu 950 - 2nd floor, 1114, Buenos Aires, Argentina.
  • Mazo T; Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires, JE Uriburu 950 - 2nd floor, 1114, Buenos Aires, Argentina.
  • Marchini T; Institute of Biochemistry and Molecular Medicine (IBIMOL UBA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
  • Caceres L; Institute of Biochemistry and Molecular Medicine (IBIMOL UBA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
  • Evelson P; Institute of Biochemistry and Molecular Medicine (IBIMOL UBA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
  • Gelpi RJ; Institute of Cardiovascular Physiopathology, Department of Pathology, Faculty of Medicine, University of Buenos Aires, JE Uriburu 950 - 2nd floor, 1114, Buenos Aires, Argentina. rgelpi@fmed.uba.ar.
Mol Cell Biochem ; 415(1-2): 67-76, 2016 Apr.
Article em En | MEDLINE | ID: mdl-26932791
Thioredoxin-1 (Trx-1) is part of an antioxidant system that maintains the cell redox homeostasis but their role on ischemic postconditioning (PostC) is unknown. The aim of this work was to determine whether Trx-1 participates in the cardioprotective mechanism of PostC in young, middle-aged, and old mice. Male FVB young (Y: 3 month-old), middle-aged (MA: 12 month-old), and old (O: 20 month-old) mice were used. Langendorff-perfused hearts were subjected to 30 min of ischemia and 120 min of reperfusion (I/R group). After ischemia, we performed 6 cycles of R/I (10 s each) followed by 120 min of reperfusion (PostC group). We measured the infarct size (triphenyltetrazolium); Trx-1, total and phosphorylated Akt, and GSK3ß expression (Western blot); and the GSH/GSSG ratio (HPLC). PostC reduced the infarct size in young mice (I/R-Y: 52.3 ± 2.4 vs. PostC-Y: 40.0 ± 1.9, p < 0.05), but this protection was abolished in the middle-aged and old mice groups. Trx-1 expression decreased after I/R, and the PostC prevented the protein degradation in young animals (I/R-Y: 1.05 ± 0.1 vs. PostC-Y: 0.52 ± .0.07, p < 0.05). These changes were accompanied by an improvement in the GSH/GSSG ratio (I/R-Y: 1.25 ± 0.30 vs. PostC-Y: 7.10 ± 2.10, p < 0.05). However, no changes were observed in the middle-aged and old groups. Cytosolic Akt and GSK3ß phosphorylation increased in the PostC compared with the I/R group only in young animals. Our results suggest that PostC prevents Trx-1 degradation, decreasing oxidative stress and allowing the activation of Akt and GSK3ß to exert its cardioprotective effect. This protection mechanism is not activated in middle-aged and old animals.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Tiorredoxinas / Traumatismo por Reperfusão Miocárdica / Fatores Etários Limite: Animals Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Argentina País de publicação: Holanda
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Tiorredoxinas / Traumatismo por Reperfusão Miocárdica / Fatores Etários Limite: Animals Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Argentina País de publicação: Holanda