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PubMed2003

Pharmacokinetics of Ginkgo biloba extracts.

EGb 761 (definition see editorial) Ginkgo extract is produced by a validated production process. Its pharmacologically active constituents, flavonol glycosides and terpene lactones, are kept within a narrow range of 22 to 27 % and 5 to 7 %, respectively, by standardisation. The concentration of ginkgolic acids is below 5 ppm. The constant production process also maintains the concentrations of other constituents such as proanthocyanidins, carboxylic acids and non-flavone glycosides at a fairly constant level. In this article, we will summarise the data on the pharmacokinetics of flavonol glycosides and terpene lactones.

Adult↗
PubMed2005

Distinct role of bilobalide and ginkgolide A in the modulation of rat CYP2B1 and CYP3A23 gene expression by Ginkgo biloba extract in cultured hepatocytes.

In the present study, primary cultures of rat hepatocytes were treated for 48 h with one of several extracts of Ginkgo biloba (10, 100, or 1000 microg/ml). Maximal increase in CYP2B1 and CYP3A23 mRNA levels was obtained at 100 microg/ml. This concentration of G. biloba extract also increased CYP3A2 and CYP3A18 mRNA expression in addition to CYP2B-mediated 7-benzyloxyresorufin O-dealkylation (BROD) and CYP3A-mediated testosterone 6beta-hydroxylation. In other experiments, cultured hepatocytes were treated for 48 h with bilobalide, ginkgolide A, ginkgolide B, ginkgolide C, ginkgolide J, kaempferol, quercetin, isorhamnetin, or a flavonol diglycoside at a concentration that represented the level present in a 100 microg/ml concentration of an extract. Only bilobalide (2.8 microg/ml) increased CYP2B1 mRNA expression, and the -fold increase (7.9 +/- 0.5; mean +/- S.E.M.) was similar to that (8.3 +/- 1.7) by the extract. By comparison, only ginkgolide A (1.1 microg/ml) increased CYP3A23 mRNA expression, but the extent (2.6 +/- 0.5-fold) was less than the 5.3 +/- 1.7-fold increase by the extract. A greater concentration (5 microg/ml) of ginkgolide A was required to elevate CYP3A2 and CYP3A18 mRNA expression. Over the range of 1 to 5 microg/ml, bilobalide increased CYP2B1 mRNA and BROD, but not CYP3A23 mRNA or testosterone 6beta-hydroxylation, whereas ginkgolide A increased CYP3A23 mRNA and testosterone 6beta-hydroxylation, but not CYP2B1 mRNA or BROD. Overall, our novel results indicate a distinct role of bilobalide and ginkgolide A in the modulation of CYP2B1 and CYP3A23 gene expression and enzyme activities by G. biloba extract in primary cultures of rat hepatocytes.

Animals↗
PubMed1996

An experimental study of the effect of ginkgo biloba extract on the human and rabbit corpus cavernosum tissue.

PURPOSE: To investigate the effect of subfractions of extract from the ginkgo on human and rabbit corpus cavernosal tissue and their possible use for the treatment of impotence. MATERIALS AND METHODS: Among the fractions of ginkgo biloba extract (GBE), nonginkgolide nonflavonoid fraction (NGF) has the most potent relaxing effect on vascular smooth muscle. We subfractionated NGF and speculated that some of the subfractions might have a very potent relaxing effect on corpus cavernosal tissue. Thereafter we have studied their effect on human and rabbit corpus cavernosum using organ bath and electrical field stimulation experiments. RESULTS: In the tissue precontracted by norepinephrine (10(-5)M.), corpus cavernosal tissue of human and rabbit showed relaxation in response to subfractions of NGF in a dose-dependent manner. 304U-1 showed the most potent relaxing effect (ED50 = 0.74 mg./ml. in human, ED50 = 0.66 mg./ml. in rabbit). 304U-1 elicits pharmacological actions on corpus cavernosum smooth muscle via the signal transduction pathway whereby relaxation induced by 304U-1 is mediated by intracellular cAMP and perhaps partially by antagonizing of the adrenergic nervous system. A hyperpolarizing effect via potassium channel opening might also be related to this relaxing effect. CONCLUSION: The subfractions of NGF, especially 304U-1, have a relaxing effect on corpus cavernosum tissue. 304U-1, which showed the most potent relaxing effect, can possibly be used as a drug for intracavernosal injection therapy. Considering the fact that the value of ED50 is too high, further fractionation and in vivo study are needed before clinical use in an oral form.

Animals↗
PubMed2006

The use of Ginkgo biloba extract in acute ischemic stroke.

BACKGROUND: Ginkgo biloba extract is widely used in the treatment of acute ischemic stroke in China. The Cochrane Re-view authors aimed to assess the evidence from randomized controlled trials and quasirandomized controlled trials on the use of Ginkgo biloba extract in acute ischemic stroke. OBJECTIVES: The primary objective is to determine whether Ginkgo biloba extract improves functional outcome without causing undue harm in patients with acute ischemic stroke. Secondary objectives are to assess the effect of Ginkgo biloba extract on neurological impairment and quality of life. SEARCH STRATEGY: The authors searched the Cochrane Stroke Group Trials Register (last searched October 2004), the Trials Register of the Cochrane Complementary Medicine Field (last searched October 2004), and the Chinese Stroke Trials Register (last searched June 2004). In addition,the authors searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 3,2004), MEDLINE (1966 to August 2004), EMBASE (1980 to June 2004), AMED(1985 to May 2002), and the China Biological Medicine Database (CBM-disk,1979 to August 2004). The authors searched relevant clinical trials and re-search registers and contacted pharmaceutical companies and researchers in an ef-fort to identify further published and unpublished studies. SELECTION CRITERIA: Randomized controlled trials or quasirandomized controlled clinical trials comparing Ginkgo biloba extract with placebo or open control(no placebo) in patients with acute ischemic stroke. DATA COLLECTION AND ANALYSIS: Two authors independently selected trials for inclusion, assessed trial quality, and extracted data. MAIN RESULTS: Fourteen trials were identified, of which 10 trials (792 patients)were included. Four trials are awaiting assessment. In the 10 included trials, follow-up was performed at 14 to 35 days after stroke. In all studies, neurological outcome was assessed, but none of them reported on disability (activities of daily living function) or quality of life. Only three trials reported adverse events. In nine trials, all of them assessed to be of inferior quality, significant improvement in neurological deficit at the end of the treatment was used as the outcome measure. When analyzing these trials together, Ginkgo biloba extract was associated with a significant increase in the number of improved patients (Peto odds ratio (OR)2.66; 95% confidence interval (CI): 1.79-3.94). One placebo-controlled trial, assessed to be of good quality, reported neurological outcome as a continuous variable. It failed to show an improvement of neurological deficit at the end of treatment (weighted mean difference (fixed)0.81; 95% CI: -8.9-10.52). No deaths or major adverse events were reported during the follow-up period. CONCLUSIONS: There was no convincing evidence from trials of sufficient methodological quality to support the routine use of Ginkgo biloba extract to promote recovery after stroke. High-quality and large-scale randomized controlled trials are needed to test its efficacy.

Activities of Daily Living↗
PubMed2001

The effect of Li 1370, extract of Ginkgo biloba, on REM sleep in humans.

Ginkgo biloba extracts (GBE) have been shown to be as effective as anti-cholinesterase inhibitors in improving the cognitive test scores of patients with dementia. Although it has been assumed that GBE works via its antioxidant and vascular effects, some evidence has emerged that GBE may have some pro-cholinergic activity. We wished to test the hypothesis that a standardised preparation of GBE, Li 1370, increases cholinergic activity by measuring its effect on the sleep polysomnogram. In particular, latency to Rapid Eye Movement (REM) sleep is sensitive to cholinergic activity. For this purpose we recruited 10 healthy volunteers of both sexes and recorded sleep polysomnograms in a randomised cross-over study, comparing sleep polysomnograms taken the night after a single evening dose of Li 1370 (240 mg) with sleep polysomnograms taken after an evening dose of placebo. No significant differences in sleep parameters (including REM sleep measures) were detected; however sleep efficiency measures and subjective sleep quality reports showed that Li 1370 was well tolerated.

Adolescent↗
PubMed2000

Efficacy and safety of a Ginkgo biloba extract.

This review of the literature documents the efficacy of a standard extract of Ginkgo biloba (EGb) in managing signs and symptoms associated with memory disorders and dementia. Analysis of the discrepant findings reveals that study outcomes may vary with the type of population studied, the outcome measurements selected, and the dosing tested. Overall, the efficacy of EGb was more frequently reported in trials enrolling dementia patients than healthy volunteers. In contrast to narrow memory tests, broad cognitive assessments were more likely to detect the treatment effect. Although a dose--response relationship is not yet established, 240 mg day(-1) EGb seems to show a higher rate of treatment response than does 120 mg day(-1). Regarding safety, in all trials reviewed the adverse event profile of EGb was not different from that of the placebo.

Antioxidants↗
PubMed2002

[Protection of synaptosomal polyunsaturated fatty acids from by extract of Ginkgo biloba-EGb 761].

Previous studies have demonstrated that ascorbic acid associated with ferrous ions induced deleterious effects on several targets or functions of striatal dopaminergic nerve endings, which were prevented by the Ginkgo biloba extract EGb 761. The present study attempted to assess whether a peroxidation of polyunsaturated fatty acids of their membranes could be associated with (or even responsible for) these alterations. Synaptosomes were prepared from mice striata. Their 1 h incubation with ascorbic acid (0.1 mM) resulted in a marked increase (+300%) of thiobarbituric acid reactive substances, that roughly are considered to correspond to the malondialydehyde level. Under these conditions the level of polyunsaturated fatty acids, measured by gas chromatography, decreased by -23% whereas the level of saturated fatty acids was not modified. Both the increase in thiobarbituric acid reactive substances and the decrease in polyunsaturated fatty acids were prevented by EGb 761 (10 micro g/ml). Similarly, the increase of TBARS was prevented by the vitamin E analogue trolox C (0.1mM) as well as by the ferrous ions chelating agent desferrioxamine (0.1mM). These data suggest that the polyunsaturated fatty acids peroxidation could be the origin of previously reported synaptosomal alterations induced by ascorbic acid/Fe(2 +).

Animals↗
PubMed1999

Inhibition of serum deprivation- and staurosporine-induced neuronal apoptosis by Ginkgo biloba extract and some of its constituents.

Previous studies have already demonstrated that some constituents of an extract of Ginkgo biloba (EGb), such as ginkgolide B and bilobalide, protect cultured neurons from hypoxia- and glutamate-induced damage. This prompted us to investigate whether they were also able to inhibit neuronal apoptosis. We induced apoptosis in cultured chick embryonic neurons as well as in mixed cultures of neurons and astrocytes from neonatal rat hippocampus by serum deprivation and staurosporine. The increase in the percentage of apoptotic chick neurons from 12% in controls to 30% after 24 h of serum deprivation was reduced to control level by EGb (10 mg/l), ginkgolide B (10 microM), ginkgolide J (100 microM) and bilobalide (1 microM). After treatment with staurosporine (200 nM) for 24 h we observed 74% apoptotic chick neurons. This percentage of apoptotic neurons was reduced to 24%, 62% and 31% in the presence of EGb (100 mg/l), ginkgolide J (100 microM) and ginkgolide B (10 microM), respectively. Bilobalide (10 microM) decreased apoptotic damage induced by staurosporine treatment for 12 h nearly to the control level. In mixed neuronal/glial cultures, the extract of EGb (100 mg/l) and bilobalide (100 microM) rescued rat neurons from apoptosis caused by serum deprivation, whereas, bilobalide (100 microM) and ginkgolide B (100 microM) reduced staurosporine-induced apoptotic damage. Ginkgolide A revealed no anti-apoptotic effect in either serum-deprived or staurosporine-treated neurons. Our results suggest that EGb and some of its constituents possess anti-apoptotic capacity and that bilobalide is the most potent constituent.

Animals↗
PubMed2000

mRNA expression profile of a human cancer cell line in response to Ginkgo biloba extract: induction of antioxidant response and the Golgi system.

Supplementation of diets with plant extracts for health and prevention of degenerative diseases is popular. However the molecular basis of their therapeutic potentials are poorly defined. We hypothesized that in vitro assays that enable quantitative analysis of the gene expression profiles combined with targeted biochemical analysis can identify the potential effects of phytochemicals. The hypothesis was tested by application of GeneChips to define mRNA expressions of a human bladder cancer cell line incubated with a flavonoid containing extract of Ginkgo biloba leaves. The analysis of the transcriptional response revealed a net activation of transcription. Functional classification of the affected mRNAs showed the largest changes in the abundance of mRNAs for intracellular vesicular transport, mitochondria, transcription and antioxidants. The transcripts for hemeoxygenase-1, mitochondrial superoxide dismutase and the regulatory subunit of gamma-glutamyl-cysteinyl synthetase and their encoded proteins were elevated. The extract also increased intracellular glutathione, the transcripts for DNA repair and synthesis, and decreased 3H-thymidine incorporation. These results demonstrate that a flavonoid containing extract initiates an adaptive transcriptional response that augments the "antioxidant status" of the cells and inhibits DNA damage. These in vitro studies using GeneChips demonstrated a promising strategy for identifying nutritional supplement induced cellular responses that may have a role in counteracting chronic human diseases.

Antioxidants↗
PubMed1999

Inhibitory effect of Ginkgo biloba extract on the expression of inducible nitric oxide synthase in endothelial cells.

Excessive production of nitric oxide (NO) may have cytotoxic effects through the formation of peroxynitrite with superoxide. The extract of Ginkgo biloba leaves (EGb) has been demonstrated to be a potent scavenger of free radicals. Although EGb has been shown recently to inhibit NO production in macrophages, its effect on NO production in endothelial cells is largely unknown. The objective of this study was to elucidate the mechanism by which EGb affects NO production in a human endothelial cell line (ECV304). After cells were incubated with EGb (10-100 microg/mL) for 2 or 4 hr, the amounts of NO metabolites released by the cells were quantitated, and cellular NOS activities were determined following the conversion of [3H]arginine to [3H]citrulline. NOS protein expression was determined by western immunoblotting analysis. mRNA levels were examined by reverse transcription-polymerase chain reaction (RT-PCR) analysis. EGb (50 microg/mL) caused a 30% reduction of NO metabolites released by endothelial cells. Following EGb treatment, cellular inducible NO synthase (iNOS) activity was reduced by 28% with a concomitant reduction in the levels of iNOS protein mass and mRNA. There was no change in the activity or protein mass of constitutive NO synthase in these cells. EGb inhibited NO production by attenuating the level of iNOS mRNA in ECV304 cells. Selective inhibition of iNOS by EGb may be therapeutically relevant in modulating NO production in endothelial cells.

Cell Line↗
PubMed2003

Down-regulation of c-jun N-terminal kinase-activator protein-1 signaling pathway by Ginkgo biloba extract in human peripheral blood T cells.

The activation of T lymphocytes contributes to inflammatory process of cardiovascular and cerebrovascular diseases. We investigated the effects of the extract of Ginkgo biloba (EGb), an ancient plant preserving antioxidant property, on phorbol 12-myristate 13-acetate+ionomycin or anti-CD3+anti-CD28 monoclonal antibodies-activated T cells. Human peripheral blood T cells were negatively selected from whole blood. Cytokines were measured by ELISA, cell surface markers by flow cytometry and the activities of transcription factors and kinases were determined by electrophoresis mobility shift assays, kinase assays and transfection assays. We showed that EGb inhibited several cytokines, including tumor necrosis factor-alpha, interleukin (IL)-2, IL-4 and interferon-gamma production from activated T cells. Electrophoresis mobility shift assay analysis indicated that EGb down-regulated activator protein-1 (AP-1) but not nuclear factor kappa B DNA-binding activity. In addition, EGb inhibited c-jun N-terminal kinase but not extracellular signal regulated protein kinase activity. The inhibitory specificity on AP-1 by EGb was also demonstrated in transfection assays. The inhibition of AP-1 signaling pathway in T cells by EGb provides a support for its efficacy in cardiovascular and cerebrovascular diseases and raises a therapeutic potential for this drug in activated T cell-mediated pathologies.

Cytokines↗
PubMedDate not supplied

[Experimental model of cerebral ischemia preventive activity of Ginkgo biloba extract (author's transl)].

Unilateral embolization of the brain was performed in rats by intracarotid injection of 4 000 radioactive microspheres (50 mu). Local blood flow in hippocampus, striatum, hypothalamus and remainder of the brain were determined using the iodoantipyrine technique. Embolization resulted in a decreases in blood flow and modificationof the distribution of microflow. Furthermore, embolization produces changes in energy metabolism : particularly a fall in ATP and glucose levels and an increase in lactate level. Subsequently, severe vasogenic edema developed. There was a correlation between the number of microspheres injected and the amount of edema. Pretreatment using an extracted of Ginkgo biloba leaves partially suppressed the effect of embolization. An improvement of the flow in the ischemic areas associated with an improvement of the energy metabolism explain the decreases of the edema.

Animals↗
PubMed1982

[Cerebral ischemia after ligature of both carotid arteries in rats: effect of ginkgo biloba extracts (author's transl)].

Simultaneous ligature of both carotid arteries in Long Evans rats results in death for all animals. 50% of the animals survive if the ligatures are separated by a four-day interval. Studies of variations in cerebral blood flow according to the time interval between the two ligatures show that alternative vascularization develops and that the balance between both hemibrains is restored. After giving L-dopa3H to animals with ligature of both carotids, increased synthesis of cerebral dopamine 3H and norepinephrine 3H can be demonstrated. When animals are given extracts of Ginkgo biloba leaves prior to carotid ligatures, survival rate is improved and dopamine synthesis increased, without marked changes in cerebral blood flow. This is related to increased brain cell activity in spite of hypoxia due to carotid ligature.

Animals↗
PubMed1984

Endothelium-dependent relaxations of rabbit isolated aorta produced by carbachol and by Ginkgo biloba extract.

Spirally-cut strips of rabbit aorta were used to examine the relaxations produced by carbachol and extract of Ginkgo biloba (Gb) under isometric conditions. After precontracting the strips with phenylephrine (10(-7) M), carbachol produced a dose-related relaxation (PD2 congruent to 6.2 +/- 0.1) and this effect was antagonized competitively by atropine (PA2 congruent to 9.4 +/- 0.1). Gb (0.2 or 0.3 mg/ml) also relaxed the strips. Removal of the endothelium or a 30-min pre-treatment of the strips with a substance that has lipoxygenase-inhibitor activity (nordihydroguaiaretic acid, NDGA, 10(-5) M) abolished the relaxant effect of carbachol and partially blocked the relaxant effect of Gb. Thus, at least part of the relaxant effect of Gb is mediated by a factor(s) (e.g., EDRF) that is released from endothelial cells.

Animals↗
PubMed1994

Myricetin and quercetin, the flavonoid constituents of Ginkgo biloba extract, greatly reduce oxidative metabolism in both resting and Ca(2+)-loaded brain neurons.

The antioxidant action of myricetin and quercetin, the flavonoid constituents of the extract of Ginkgo biloba (EGb), on oxidative metabolism of brain neurons dissociated from the rats was examined using 2',7'-dichlorofluorescin (DCFH) which is retained within the neuron and then is oxidized by cellular hydrogen peroxide to be highly fluorescent. Incubation with myricetin or quercetin reduced the oxidation of DCFH in resting brain neurons, more profoundly than EGb. Myricetin decreased the oxidative metabolism at concentrations of 3 nM or more. It was 10 nM or more for the case of quercetin. Incubation with each flavonoid constituent also reduced the Ca(2+)-induced increase in the oxidative metabolism without affecting the cellular content of DCFH or the intracellular concentrations of Ca2+. Such an antioxidant action of myricetin or quercetin may be responsible for a part of the beneficial effects of EGb on brain neurons subject to ischemia.

Animals↗
PubMed1995

Identification of flavonoid metabolites after oral administration to rats of a Ginkgo biloba extract.

An extract of Ginkgo biloba leaves (EGb) was administered by gastric probe to Wistar female rats, and urine and faeces samples were collected for 5 days and whole blood samples were withdrawn every 30 min for 6 h. After purification with SPE C18 cartridges, the samples were analysed by reversed-phase LC-diode array detection (LC-DAD) for residual flavonoid glycosides, aglycones and metabolites. No glycosides or aglycones were detected in urine, faeces or blood and extensive degradation of EGb flavonoids within 24 h was detected. Among the seven different phenylalkyl acids detected by LC-DAD, 3,4-dihydroxyphenylacetic acid (I), hippuric acid (II), 3-hydroxyphenylacetic acid (III), homovanillic acid (IV) and benzoic acid (VII) were directly confirmed by on-line mass spectrometry using an electrospray interface (ES-MS). Peaks V and VI needed to be collected and separately examined and they were found to be 3-(4-hydrophenyl)propionic acid and 3-(3-hydrophenyl)propionic acid, respectively. As further evidence, the identity of metabolites I, II, III, IV, V and VII was confirmed by co-chromatography with authentic standards.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Effects of Ginkgo biloba extract on glucose transport and glycogen synthesis of cultured smooth muscle cells from pig aorta.

We have examined the effect of an extract of Ginkgo biloba (Gbe) on glucose uptake and on glycogen synthesis in cultured smooth muscle cells (SMC) from pig aorta. Initial rates of glucose transport were determined by measurements of 2-deoxy-D-glucose (2-DG) uptake. From kinetic analyses apparent KM and Vmax values of facilitated glucose transport in cultured SMC were evaluated at 2.2 mM and 9.1 nmol/min/10(6) cells respectively. Gbe stimulated glucose transport in a dose-dependent manner; the maximum effect was reached at a Gbe concentration of 0.25 micrograms/ml and represented an increase of 35 +/- 4% above basal activity. This stimulation mainly occurred on facilitated glucose transport. The passive diffusion measured when cells were treated with cytochalasin B represented 15 +/- 3% of glucose total transport activity either in the absence or the presence of Gbe. The effect of Gbe on glycogen synthesis in cultured SMC was then tested by the incorporation of U14C-glucose into cellular glycogen. This process was enhanced by Gbe, the maximal effect was observed at a Gbe concentration of 0.25 micrograms/ml, and represented a 41 +r4% increase above basal activity. These data argue for a direct effect of Gbe upon glucose transport and glucose utilization in cultured SMC thus allowing a better nutriment disposal in the vascular wall.

Animals↗
PubMed1985

Effects of an extract of Ginkgo biloba on noradrenergic systems of rat cerebral cortex.

Oral treatment of rats with Ginkgo biloba extract (Gb) elicited a biphasic effect on normetanephrine (NMN) content of cerebral cortex; an initial decrease was evident after 45 minutes, followed by a marked increase that was evident after 14 days. Chronic treatment with Gb led to decreases in the density of 3H-dihydroalprenolol binding (after 27 days or 2 months) and in isoproterenol-stimulated adenylate cyclase activity (after 2 months) of the cerebral cortex. Taken together, these results indicate that the effects of Gb on the central beta-adrenergic system might be involved in its therapeutic actions.

Adenylyl Cyclases↗