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

共 45 条

[31] MITOCHONDRIAL-FUNCTION IN THE OXYGEN DEPLETED AND REOXYGENATED MYOCARDIAL-CELL [J].

PIPER, HM ;

NOLL, T ;

SIEGMUND, B .

CARDIOVASCULAR RESEARCH, 1994, 28 (01) :1-15

[32] MITOCHONDRIAL DAMAGE DURING MYOCARDIAL ISCHEMIA [J].

REGITZ, V ;

PAULSON, DJ ;

HODACH, RJ ;

LITTLE, SE ;

SCHAPER, W ;

SHUG, AL .

BASIC RESEARCH IN CARDIOLOGY, 1984, 79 (02) :207-217

[33] MITOCHONDRIAL COMPLEX-I, COMPLEX-II, COMPLEX-III, COMPLEX-IV, AND COMPLEX-V, IN MYOCARDIAL ISCHEMIA AND AUTOLYSIS [J].

ROUSLIN, W .

AMERICAN JOURNAL OF PHYSIOLOGY, 1983, 244 (06) :H743-H748

[34] LOCALIZATION OF MITOCHONDRIAL CREATINE KINASE, AND ITS USE FOR DETERMINATION OF SIDEDNESS OF SUBMITOCHONDRIAL PARTICLES [J].

SCHOLTE, HR ;

WEIJERS, PJ ;

WITPEETE.EM .

BIOCHIMICA ET BIOPHYSICA ACTA, 1973, 291 (03) :764-773

[35] BIOCHEMICAL AND MORPHOLOGIC CORRELATES OF CARDIAC ISCHEMIA .1. MEMBRANE SYSTEMS [J].

SCHWARTZ, A ;

WOOD, JM ;

ALLEN, JC ;

BORNET, EP ;

ENTMAN, ML ;

GOLDSTEIN, MA ;

SORDAHL, LA ;

SUZUKI, M .

AMERICAN JOURNAL OF CARDIOLOGY, 1973, 32 (01) :46-61

[36]

SHEN JG, 1995, BIOCHEM MOL BIOL INT, V35, P125

[37]

Shug A L, 1975, Recent Adv Stud Cardiac Struct Metab, V10, P365

[38] The importance of scavenging reactive oxygen species in anti-aging medicine [J].

Siegel, Guenter ;

Schmidt, Annette ;

Schaefer, Petra ;

Malmsten, Martin ;

Ringstad, Lovisa ;

Winkler, Karl ;

Just, Soeren .

ENGINEERING IN LIFE SCIENCES, 2009, 9 (05) :363-375

[39] New data on biochemical mechanism of programmed senescence of organisms and antioxidant defense of mitochondria [J].

Skulachev, V. P. .

BIOCHEMISTRY-MOSCOW, 2009, 74 (12) :1400-1403

[40] Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion [J].

Solaini, G ;

Harris, DA .

BIOCHEMICAL JOURNAL, 2005, 390 :377-394

← 1 2 3 4 5 →