The Effect of Ginkgo biloba Extract on Mitochondrial Oxidative Phosphorylation in the Normal and Ischemic Rat Heart

被引：11

作者：

Bernatoniene, Jurga ^{[1
]}

Majiene, Daiva ^{[1
,2
]}

Peciura, Rimantas ^{[1
]}

Laukeviciene, Ale ^{[3
]}

Bernatoniene, Ruta ^{[4
]}

Mekas, Tauras ^{[1
]}

Kasauskas, Arturas ^{[5
]}

Kopustinskiene, Dalia ^{[2
,5
]}

机构：

[1] Kaunas Univ Med, Dept Drug Technol & Social Pharm, LT-44307 Kaunas, Lithuania

[2] Kaunas Univ Med, Biomed Res Inst, LT-50009 Kaunas, Lithuania

[3] Kaunas Univ Med, Dept Physiol, LT-44307 Kaunas, Lithuania

[4] Kaunas Univ Med, Dept Pharmaceut Chem, LT-44307 Kaunas, Lithuania

[5] Kaunas Univ Med, Dept Biochem, LT-50009 Kaunas, Lithuania

来源：

PHYTOTHERAPY RESEARCH | 2011年 / 25卷 / 07期

关键词：

Ginkgo biloba; heart mitochondrial respiration; ischemic injury; cardioprotection; MYOCARDIAL-ISCHEMIA; EGB; 761; REPERFUSION INJURY; KINETIC-ANALYSIS; RESPIRATION; PROTECTION; OXYGEN; MECHANISM; SYSTEM; DAMAGE;

D O I：

10.1002/ptr.3399

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

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 (C) 2011 John Wiley & Sons, Ltd.

引用

页码：1054 / 1060

页数：7

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