학술논문

Abstract 13999: Daily CoQ10 Administration Enhances Expression of Electron Transport Chain Proteins in Hibernating Myocardium
Document Type
Academic Journal
Source
Circulation. Nov 14, 2017 136(Suppl_1 Suppl 1):A13999-A13999
Subject
Language
English
ISSN
0009-7322
Abstract
Introduction: Coenzyme Q10 (CoQ10) has been shown to reduce oxidant stress in ischemic heart tissue, though it is unclear whether it alters the expression of electron transport chain (ETC) proteins within mitochondria from the ischemic territory.Hypothesis: Using a swine model of chronic myocardial ischemia, we tested whether daily administration of CoQ10for 4-weeks would enhance the expression of ETC proteins in mitochondria from the chronically ischemic regions.Methods: Twelve pigs underwent placement of a constrictor around the LAD artery and had reduced regional function at 12 weeks. Pigs were given daily dietary supplements of either CoQ10 (10 mg/kg/day) or placebo and studied with 2-D ECHO 4 weeks later. Animals were sacrificed and mitochondria were isolated from the LAD regions, for analysis of ETC proteins by western gels and oxidant stress markers by a protein carbonyl assay.Results: At 12 weeks following instrumentation, regional wall thickening in the LAD region of the Placebo and CoQ10 regions was lower than remote regions (34±7% versus 62±7%; P<0.01), consistent with the presence of chronic myocardial ischemia. Following 4-weeks of treatment, repeat estimates of regional wall thickening in the LAD and Remote regions were 41±5% versus 72±7% (P<0.01), suggesting minimal change in regional function. Post-sacrifice, mitochondria were isolated from the ischemic regions and analyzed for ETC protein expression. As shown in the Figure, the CoQ10 treated-pigs demonstrated higher levels of ETC proteins, particularly Complex V compared with Placebo treated pigs.Conclusions: In summary, in this model of chronic myocardial ischemia, supplementation with CoQ10 at 4 weeks improves the expression of ETC proteins in the mitochondria, potentially by reducing oxidant stress in the mitochondria.