Stabilization of mitochondrial membrane potential and improvement of neuronal energy metabolism by Ginkgo biloba extract EGb 761

被引:92
作者
Eckert, A [1 ]
Keil, U
Scherping, I
Hauptmann, S
Müller, WE
机构
[1] Univ Basel, Psychiat Clin, Neufeld Cardiac Res Inst, Neurobiol Res Lab, CH-4025 Basel, Switzerland
[2] Univ Frankfurt, Bioctr, Dept Pharmacol, D-60439 Frankfurt, Germany
来源
NATURAL PRODUCTS AND MOLECULAR THERAPY | 2005年 / 1056卷
关键词
Ginkgo biloba; mitochondria; energy metabolism; Alzheimer's disease; aging; oxidative stress;
D O I
10.1196/annals.1352.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ginkgo biloba extract EGb 761 has been used for many years to treat age-related cognitive disorders including Alzheimer's disease. EGb 761 given shortly after initiating mitochondrial damage by sodium nitroprusside (nitric oxide donor) improved the mitochondrial membrane potential of PC12 cells significantly and dose dependently. Under these conditions, EGb 761 also reversed the decrease in ATP production. In addition, similar protection against oxidative damage was found in dissociated brain cells and isolated brain mitochondria after in vitro or in vivo treatment with EGb 761. Moreover, PC12 cells bearing an Alzheimer's disease-related mutation in the amyloid precursor protein, which leads to enhanced beta amyloid production, showed greater benefit from treatment with EGb 761 than did control cells. Taken together, our findings clearly show stabilization and protection of mitochondrial function as a specific and very sensitive property of EGb 761 at therapeutically relevant doses.
引用
收藏
页码:474 / 485
页数:12
相关论文
共 64 条
[1]   Mitochondrial targeting and a novel transmembrane arrest of Alzheimer's amyloid precursor protein impairs mitochondrial function in neuronal cells [J].
Anandatheerthavarada, HK ;
Biswas, G ;
Robin, MA ;
Avadhani, NG .
JOURNAL OF CELL BIOLOGY, 2003, 161 (01) :41-54
[2]   Rhodamine 123 as a probe of mitochondrial membrane potential:: evaluation of proton flux through F0 during ATP synthesis [J].
Baracca, A ;
Sgarbi, G ;
Solaini, G ;
Lenaz, G .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2003, 1606 (1-3) :137-146
[3]   Mitochondria, free radicals, and neurodegeneration [J].
Beal, MF .
CURRENT OPINION IN NEUROBIOLOGY, 1996, 6 (05) :661-666
[4]   IMMUNOCYTOCHEMICAL DEMONSTRATION OF CYTOCHROME-C OXIDASE WITH AN IMMUNOPEROXIDASE METHOD - A SPECIFIC STAIN FOR MITOCHONDRIA IN FORMALIN-FIXED AND PARAFFIN-EMBEDDED HUMAN-TISSUES [J].
BEDETTI, CD .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1985, 33 (05) :446-452
[5]   Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease [J].
Bosetti, F ;
Brizzi, F ;
Barogi, S ;
Mancuso, M ;
Siciliano, G ;
Tendi, EA ;
Murri, L ;
Rapoport, SI ;
Solaini, G .
NEUROBIOLOGY OF AGING, 2002, 23 (03) :371-376
[6]   The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761) in rats [J].
Bridi, R ;
Crossetti, FP ;
Steffen, VM ;
Henriques, AT .
PHYTOTHERAPY RESEARCH, 2001, 15 (05) :449-451
[7]   Nitric oxide inhibition of mitochondrial respiration and its role in cell death [J].
Brown, GC ;
Borutaite, V .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (11) :1440-1450
[8]   Mitochondrial free radical generation, oxidative stress, and aging [J].
Cadenas, E ;
Davies, KJA .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (3-4) :222-230
[9]   β-amyloid fragment 25-35 selectively decreases complex IV activity in isolated mitochondria [J].
Canevari, L ;
Clark, JB ;
Bates, TE .
FEBS LETTERS, 1999, 457 (01) :131-134
[10]   Cytochrome c oxidase is decreased in Alzheimer's disease platelets [J].
Cardoso, SM ;
Proença, MT ;
Santos, S ;
Santana, I ;
Oliveira, CR .
NEUROBIOLOGY OF AGING, 2004, 25 (01) :105-110