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The Effect of Ginkgo biloba Extract on Mitochondrial Oxidative Phosphorylation in the Normal and Ischemic Rat Heart
Author(s) -
Bernatoniene Jurga,
Majiene Daiva,
Peciura Rimantas,
Laukeviciene Ale,
Bernatoniene Ruta,
Mekas Tauras,
Kasauskas Arturas,
Kopustinskiene Dalia
Publication year - 2011
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3399
Subject(s) - ginkgo biloba , mitochondrion , oxidative phosphorylation , respiration , ischemia , pharmacology , cytochrome c , ethanol , biochemistry , chemistry , medicine , endocrinology , anatomy
Free radical‐induced myocardial damage and impairment of vascular endothelium‐dependent relaxation are amongst the most important mechanisms responsible for ischemic heart injury. Ginkgo biloba leaf extract (GE) has been reported to improve blood circulation in the brain and have a beneficial impact on the cardiovascular system but its cardioprotective effects have not been elucidated yet. Therefore, this study investigated the influence of GE in 70% ethanol (1:5) administered orally to rats on the functions of isolated heart mitochondria under normal and ischemic conditions. Wistar rats were given GE or ethanol (solvent control) at a dosage of 0.32 mL/kg in drinking water for 10 and 18 days, while the control animals received untreated drinking water. Mitochondrial respiration rates were determined oxygraphically. Pyruvate and malate, succinate or palmitoyl‐ l ‐carnitine and malate were used as substrates. The GE treatment partially uncoupled mitochondrial oxidation from phosphorylation, reduced the generation of free radicals in the mitochondria, diminished the ischemia‐induced V 3 decrease and the degree of respiration stimulation by exogenous cytochrome c. Thus, these results indicate that GE exerts cardioprotective effects reducing ischemia‐caused impairment of the functions of heart mitochondria. Copyright © 2011 John Wiley & Sons, Ltd.