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  • Title: Long-term oral resveratrol intake provides nutritional preconditioning against myocardial ischemia/reperfusion injury: involvement of VDAC1 downregulation.
    Author: Liao Z, Liu D, Tang L, Yin D, Yin S, Lai S, Yao J, He M.
    Journal: Mol Nutr Food Res; 2015 Mar; 59(3):454-64. PubMed ID: 25488258.
    Abstract:
    SCOPE: This study elucidates the effects of long-term nutritional preconditioning by resveratrol on ischemia/reperfusion (I/R) injury and its underlying mechanisms. METHODS AND RESULTS: Mice were treated with resveratrol at 2.0 mg/kg/day by gastric gavages for 6 wk. Then hearts were isolated and subjected to I/R injury in a Langendorff apparatus. Resveratrol significantly improved left ventricular pressure, ±dp/dtmax, and coronary flow; decreased the lactate dehydrogenase and creatine phosphokinase activities; and reduced the infarction size. Additionally, long-term oral resveratrol intake prevented mitochondrial permeability transition pore opening and subsequently inhibited mitochondria-mediated apoptosis, as demonstrated by decrease of cytochrome c release, inactivation of caspase-3, and reduction of terminal deoxynucleotidyl transferase mediated nick end labeling positive cells. Furthermore, resveratrol inhibited the upregulation of voltage-dependent anion channel 1 (VDAC1) expression induced by I/R injury. Local left-ventricle overexpression of VDAC1 by adenovirus diminished the protective effect of resveratrol against I/R injury, indicating that VDAC1 plays an important role in resveratrol-mediated cardioprotection. CONCLUSION: Our data revealed that long-term oral intake of resveratrol sets nutritional preconditioning to cope with myocardial I/R injury. Strikingly, we found that resveratrol downregulates VDAC1, leading to prevention of mitochondrial permeability transition pore opening and cardiomyocyte apoptosis.
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