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    • Adiponectin Attenuates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury Through Inhibition of Endoplasmic Reticulum Stress

      2011, 19(3):274-275.

      Keywords:AdiponectinHypoxia-ReoxygenationEndoplasmic Reticulum Stressp38 Mitogen-Activated Protein Ki-naseCell Death
      Abstract (1197)HTML (0)PDF 1.76 M (1219)Favorites

      Abstract:Background and Aim Adiponectin(APN) is a potent cardioprotective molecule.The present study aims to investigate the under-lying mechanism(s) for its cardioprotective effect.Methods Primary cardiomyocytes were isolated from neonatal rats and an invitro model of hypoxia-reoxygenation(H/R) was established.The cardiomyocytes were randomly divided into six groups: salinegroup(control),dithiothreitol(DTT) group(5 mmol/L DTTfor 2 h),H/R group,H/R +APN group(incubation with 30 mg/LAPN,followed by H/R),H/R +APN +SB203580(SB) group(treatment with 30 mg/L APN and 5μmol/L SB,followed by H/R),and H/R +SB group(exposure to 5μmol/L SB and then H/R).Cell death was detected by measuring lactate dehydrogenase(LDH) release.The expression levels of hypoxia-inducible factor-1alpha(HIF-1α) and endoplasmic reticulum(ER) stress-relatedgenes including GRP78,caspase-12,C/EBP homologus protein(CHOP),and p38 mitogen-activated protein kinase(MAPK) wereexamined.Results Cardiomyocytes exposed to H/R showed a significant increase in LDH leakage and HIF-1αprotein levelscompared with the control cells(p<0.05).The H/R-provoked cell death was profoundly attenuated by the pretreatment with APNalone,SB alone,or both,which was coupled with decreased expression of GRP78,caspase-12,CHOP,and p38 MAPK.Conclu-sions These results provide new insights into the mechanism of APN-mediated cardioprotection,which may be partially due to inhibi-tion of ER stress response.

    • Post-hypoxia Reoxygenation Enhanced Glucose Oxidation Effect and Fatty Acid Oxidation Effect of Hypertrophied Cardiomyocyte

      2010, 18(5):363-366.

      Keywords:Hypoxia-ReoxygenationHypertrophied CardiomyocytesEnergy Metabolism
      Abstract (1064)HTML (0)PDF 4.50 M (907)Favorites

      Abstract:Aim To explore effects of hypoxia-reoxygenation on glucose oxidation and fatty acid oxidation(FAO) of hypertrophied cardiomyocytes. Methods Cultured rat cardiomyocytes were induced to be hypertrophy by angiotention Ⅱ(AngⅡ) and norepinephrine(NE),which was confirmed by -Leu incorporation in cardiomyocytes and detection surface area of cells.We established a model of post-hypoxia reoxygenation of cultured cardic cells in vitro.Glucose oxidation,FAO and acitivity of pyruvate dehydrogenase(PDH) and carnitine palmitoyltransferase(CPT) were determined by liquid scintillation counting. Results Surface area of cells increased by 63.94% and -Leu incorporation by 181.54%,when 0.1 μmol/L Ang Ⅱand 1 μmol/L NE were added in vitro.Activity of PDH decreased,and glucose oxidation decreased by 48%;Activity of PDH and glucose oxidation recovered to the level of prehypoxia at 8 hours of reoxygenation.Activity of CPT decreased,and FAO decreased by 60%;Activity of FAO and CPT recovered gradually to the level of prehypoxia during reoxygenation. Conclusion Glucose oxidation and fatty acid oxidation of hypertrophied cardiomyocyte decreased during hypoxia,and both recovered during reoxygenation.Activity of PDH and CPT was involved in these changes.

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