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PubMed1993

Ca(2+)-induced increase in oxidative metabolism of dissociated mammalian brain neurons: effect of extract of ginkgo biloba leaves.

Effect of an extract of Ginkgo biloba leaves (EGb) on oxidative metabolism was studied using rat brain neurons and 2',7'-dichlorofluorescin fluorescence. Ionomycin (100 nM to 1 microM), a Ca(2+)-ionophore, dose-dependently augmented the 2',7'-dichlorofluorescin fluorescence in the presence of external Ca2+, but not under the external Ca(2+)-free condition. Preincubation of neurons with EGb (3 micrograms/ml) greatly reduced the ionomycin-induced increase in 2',7'-dichlorofluorescin fluorescence. Results suggest that EGb may reduce the Ca(2+)-induced increase in the oxidative metabolism of brain neurons.

Animals↗
PubMed2003

[Determination of ginkgolic acids in Ginkgo biloba extract and its preparations by high performance liquid chromatography].

AIM: To establish a high performance liquid chromatographic method for determination of ginkgolic acids in Ginkgo biloba extract and its preparations. METHODS: Ginkgo biloba extract and its preparations were extracted with petroleum ether in Soxhlet apparatus, and then concentrated under vacuum. The ginkgolic acids were determined directly by HPLC, and identified by LC/DAD/ESI/MS. The chromatographic column was Inertsil ODS-2; the mobile phase was methanol-3% aqueous acetic acid(92:8); the flow rate was 1.0 mL.min-1; the column temperature was 40 degrees C; the detection wavelength was 310 nm. RESULTS: There were six kinds of ginkgolic acid (C13:0, C15:1, C17:2, C15:0, C17:1 and an unknown compound C17:3 tentatively) in the Ginkgo biloba extract. The relative percentage content of ginkgolic acids C13:0, C15:1 and C17:1 was above 94%. The content of ginkgolic acids in Ginkgo biloba extract containing high content ginkgolic acids was 1.12%, and RSD was 2.4% (n = 5). The content of ginkgolic acids in one kind of EGb preparations (tablet) was 49.2 micrograms.g-1, and RSD was 4.3% (n = 5). The average recovery was 98.2%, RSD was 2.6% (n = 5). CONCLUSION: The method is accurate, fast, simple, and can be used for determination of ginkgolic acids in Ginkgo biloba extract and its preparations.

Chromatography, High Pressure Liquid↗
PubMed1986

[Absorption, distribution and elimination of a labelled extract of Ginkgo biloba leaves in the rat].

The absorption, distribution and elimination of a radiolabelled 14C extract prepared from Ginkgo biloba leaves have been studied in rats. Following oral administration, expired 14C-CO2 represented 16% of the administered dose excreted within the first 3 hours post-dose out of a total of 38% after 72 hours. An additional 21% of the administered dose was eliminated in the urine. The absorption of the radiolabelled Ginkgo biloba extract was at least 60%. The pharmacokinetics of the drug, based on blood specific activity data versus time course, were characteristic of a two-compartment model with an apparent first order phase and a biological half-life of approximatively 4.5 h. During the first 3 hours, radioactivity was primarily associated with the plasma, but through a gradual uptake after 48 h. The specific activity in erythrocytes matched that of plasma. A site of absorption in the upper gastrointestinal tract is suspected since specific activity in blood peaked after 1.5 hours. Glandular and neuronal tissues and eyes showed a high affinity for the labelled substance. These results provide the first tentative link between the therapeutic effectiveness of Ginkgo biloba extract and the biological fate of some of its constituents.

Animals↗
PubMed2000

An examination of the efficacy of Ginkgo biloba extract EGb761 on the neuropsychologic functioning of cognitively intact older adults.

OBJECTIVES: Few investigations have examined the effectiveness of Ginkgo biloba extract for enhancing cognitive abilities in individuals with no history of significant neurocognitive dysfunction. The purpose of this research was to examine the relatively short-term (i.e., 6 weeks) efficacy of Ginkgo biloba extract EGb 761 on the cognitive functioning of cognitively intact persons over the age of 55 years via a diverse battery of neuropsychologic tests and measures. PARTICIPANTS: From the 48 cognitively intact participants between the ages of 55 and 86 years who initially enrolled in this study, 21 males and 19 females successfully completed the study's protocol and provided valid data sets. DESIGN: A 6-week, double-blind, fixed-dose, placebo-controlled, parallel-group experimental design was utilized. Participants were randomly assigned to either a Ginkgo biloba extract EGb 761 (180 mg/d) or placebo control group. To evaluate participants' cognitive and behavioral functioning, series of neuropsychological tests were administered to them prior to the initiation of the Ginkgo biloba extract/placebo therapy (i.e., pretreatment baseline) and again, just prior to the termination of the treatment regimen (i.e., after 6 weeks). RESULTS: Participants who received 180 mg of Ginkgo biloba extract EGb 761 daily for 6 weeks exhibited significantly more improvement on a task assessing speed of processing abilities (i.e., Stroop Color and Word Test color-naming task) by the end of treatment as compared to participants who received placebo. Trends favoring improved performances in the Ginkgo biloba group were also demonstrated in three of the four remaining tasks that involved a timed, speed of processing component, although they did not reach statistical significance. Furthermore, a significant relationship was found between the type of treatment (Ginkgo biloba extract or placebo) and participants' ratings of their overall abilities to remember. Specifically, more participants in the Ginkgo biloba extract group rated their overall abilities to remember by the end of treatment as "improved," as compared to the placebo group. In contrast, no significant differences were found between the Ginkgo biloba and placebo groups by treatment end on any of the four objective memory measures. CONCLUSIONS: Taken together, the findings from standardized neuropsychologic assessment and a subjective, self-report questionnaire suggested that relatively short-term (i.e., 6 weeks) utilization of Ginkgo biloba extract EGb 761 may prove efficacious in enhancing certain neurocognitive functions/processes of cognitively intact older adults.

Aged↗
PubMed1993

Visual evoked potentials and optic nerve histopathology in normal and diabetic rats and effect of ginkgo biloba extract.

The purpose of this study was to test the possible therapeutic role of ginkgo biloba extract on the impairment of visual function and pathological histology of the optic nerve caused by early diabetes. Ginkgo biloba extract entraps oxygenated free radicals and is also a strong inhibitor of the platelet activation factor (PAF). For this purpose, VEP recordings and optic nerve histopathology were studied on alloxan diabetic and normal Swiss albino rats in four experimental groups. The VEP recordings showed no statistical significance between diabetic and normal rats. However, the amplitudes were significantly increased in diabetic animals with ginkgo biloba extract compared with the diabetics, supposing an impression of axonal protection. But the amplitude values were decreased in normal rats treated with the same extract compared with normal animals, assuming a toxic activity. Optic nerve ultrastructural findings also confirmed these VEP changes. It was concluded that this extract could be encouraging for human clinical trials of diabetes.

Administration, Oral↗
PubMed2002

Inhibition of amyloid-beta aggregation and caspase-3 activation by the Ginkgo biloba extract EGb761.

Standardized extract from the leaves of the Ginkgo biloba tree, labeled EGb761, has been used in clinical trials for its beneficial effects on brain functions, particularly in connection with age-related dementias and Alzheimer's disease (AD). Substantial experimental evidence indicates that EGb761 protects against neuronal damage from a variety of insults, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing an AD-associated double mutation, we report that EGb761 inhibits formation of amyloid-beta (Abeta) fibrils, which are the diagnostic, and possibly causative, feature of AD. The decreased Abeta fibrillogenesis in the presence of EGb761 was observed both in the conditioned medium of this Abeta-secreting cell line and in solution in vitro. In the cells, EGb761 significantly attenuated mitochondrion-initiated apoptosis and decreased the activity of caspase 3, a key enzyme in the apoptosis cell-signaling cascade. These results suggest that (i) neuronal damage in AD might be due to two factors: a direct Abeta toxicity and the apoptosis initiated by the mitochondria; and (ii) multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of Abeta aggregation, underlie the neuroprotective effects of EGb761.

Alzheimer Disease↗
PubMed2004

Effects of Ginkgo biloba extract on cell proliferation and cytotoxicity in human hepatocellular carcinoma cells.

AIM: To study the effect of Ginkgo biloba extract (EGb 761) containing 22-27% flavonoids (ginkgo-flavone glycosides) and 5-7% terpenoids (ginkgolides and bilobalides) on cell proliferation and cytotoxicity in human hepatocellular carcinoma (HCC) cells. METHODS: Human HCC cell lines (HepG2 and Hep3B) were incubated with various concentrations (0-1 000 mg/L) of EGb 761 solution. After 24 h incubation, cell proliferation and cytotoxicity were determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and lactate dehydrogenase (LDH) release, respectively. After 48 h incubation, the expression of proliferating cell nuclear antigen (PCNA) and p53 protein was measured by Western blotting. RESULTS: The results showed that EGb 761 (50-1 000 mg/L) significantly suppressed cell proliferation and increased LDH release (P<0.05) in HepG2 and Hep3B cells compared with the control group. The cell proliferation of HepG2 and Hep3B cells treated with EGb 761 (1 000 mg/L) was 45% and 39% of the control group (P<0.05), respectively. LDH release of HepG2 cells without and with EGb 761 (1 000 mg/L) treatment was 6.7% and 37.7%, respectively, and that of Hep3B cells without and with EGb 761 (1 000 mg/L) treatment was 7.2% and 40.3%, respectively. The expression of PCNA and p53 protein in HepG2 cells treated with EGb 761 (1 000 mg/L) was 85% and 174% of the control group, respectively. CONCLUSION: Ginkgo biloba extract significantly can suppress proliferation and increase cytotoxicity in HepG2 and Hep3B cells. Additionally, Ginkgo biloba extract can decrease PCNA and increase p53 expression in HepG2 cells.

Carcinoma, Hepatocellular↗
PubMed2005

Extract of Ginkgo biloba leaves reverses yohimbine-induced spatial working memory deficit in rats.

Extract of Ginkgo biloba is used to alleviate age-related decline in cognitive function, which may be associated with the loss of catecholamines in the prefrontal cortex. The purpose of this study was to verify whether alpha-2 adrenergic activity is involved in the facilitative effects of extract of Ginkgo biloba on prefrontal cognitive function. Male Wistar rats were trained to reach criterion in the delayed alternation task (0, 25, and 50-s delay intervals). A pilot study found that 3 or 4 mg/kg of yohimbine (intraperitoneal) reduced the choice accuracy of the delayed alternation task in a dose and delay-dependent manner, without influencing motor ability or perseverative behaviour. Acute oral pre-treatment with doses of 50, 100, or 200 mg/kg (but not 25 mg/kg) of extract of Ginkgo biloba prevented the reduction in choice accuracy induced by 4 mg/kg yohimbine. These data suggest that the prefrontal cognition-enhancing effects of extract of Ginkgo biloba are related to its actions on alpha-2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1999

Ginkgo biloba extract increases ocular blood flow velocity.

We evaluated a possible therapeutic effect of Ginkgo biloba extract (GBE) on glaucoma patients that may benefit from improvements in ocular blood flow. A Phase I cross-over trial of GBE with placebo control in 11 healthy volunteers (8 women, 3 men: Age; 34 +/- 3 years, mean +/- SE) was performed. Patients were treated with either GBE 40 mg or placebo three times daily orally, for 2 days. Color Doppler imaging (Siemens Quantum 2000) was used to measure ocular blood flow before and after treatment. There was a two week washout period between GBE and placebo treatment. Ginkgo biloba extract significantly increased end diastolic velocity (EDV) in the ophthalmic artery (OA) (baseline vs GBE-treatment; 6.5 +/- 0.5 vs 7.7 +/- 0.5 cm/sec, 23% change, p=0.023), with no change seen in placebo (baseline vs GBE-treatment; 7.2 +/- 0.6 vs 7.1 +/- 0.5 cm/sec, 3% change, p=0.892). No side effects related to GBE were found. Ginkgo biloba extract did not alter arterial blood pressure, heart rate, or IOP. Ginkgo biloba extract significantly increased EDV in the OA and deserves further investigation in ocular blood flow and neuroprotection for possible application to the treatment of glaucomatous optic neuropathy as well as other ischemic ocular diseases.

Adult↗
PubMed2004

[Effects of the flavonoid fraction from Ginkgo biloba extract on the postprandial blood glucose elevation in rats].

The present study investigated the effects of Ginkgo biloba extract and its flavonoid fractions on alpha-amylase and alpha-glucosidase activity in vitro. Ginkgo biloba extracts and their flavonoid fraction significantly inhibited alpha-amylase and alpha-glucosidase activity in vitro. Furthermore, Ginkgo biloba extracts and their flavonoid fraction reduced the elevation of rat plasma glucose level after oral administration of various saccharinity agents. In addition, we examined the effects of the flavonoid fraction isolated from Ginkgo biloba extracts on the plasma glucose level in streptozotocin-induced diabetic rats. When flavonoid fractions were orally administered to the rats three times daily for 9 days, plasma glucose concentrations were decreased compared with those in the water treatment group. Furthermore, flavonoid fractions reduced the elevation of rat plasma glucose levels after oral administration of sucrose and glucose in streptozotocin-induced diabetic rats.

Animals↗
PubMed2001

Induction of heme oxygenase-1 by Ginkgo biloba extract but not its terpenoids partially mediated its protective effect against lysophosphatidylcholine-induced damage.

In this study, we examined whether Ginkgo Biloba Extract and its terpenoid constituents protect against oxidative stress through actions on heme oxygenase (HO) gene expression and activity. HO-1 and glutathione peroxidase (GPx) gene expressions were examined by reverse transcription polymerase chain reaction (RT-PCR) analysis, HO activity and GPx enzyme activity were analysed by spectrophotometric assay. Pretreatment of H9c2 myocytes with 100-500 microgml(-1)Ginkgo Biloba Extract caused induction of HO-1 gene expression and a significant increase in HO activity; 30 microgml(-1)ginkgolide B and 30 microgml(-1)bilobalide had little effect. Treatment with Ginkgo Biloba Extract for 24 h also significantly increased GPx gene expression and GPx enzyme activity. Pretreatment with Ginkgo Biloba Extract, ginkgolide B and bilobalide protected myocytes against lysophosphatidylcholine (LPC)-induced damage. The protective effect of Ginkgo Biloba Extract against LPC-induced damage was partially suppressed by a HO inhibitor, Zinc protoporphyrin-IX (ZnPP-IX), while ZnPP-IX did not suppress the protective effect of ginkgolide B or bilobalide. Furthermore, pretreatment with hemin, biliverdin or bilirubin reduced cytotoxicity induced by LPC. These results suggest that induction of HO-1 by Ginkgo Biloba Extract but not its terpenoid constituents may play a beneficial role in oxidative stress. The mechanism of Ginkgo Biloba Extract-induced HO-1 gene expression and the increase in HO activity may be related to alteration of intracellular glutathione levels.

Animals↗
PubMed2000

Ginkgo biloba extract ameliorates gentamicin-induced nephrotoxicity in rats.

The effect of Ginkgo biloba (EGb), a plant extract with an antioxidant effect, has been studied on gentamicin-induced nephrotoxicity in male wistar rats. Ginkgo biloba extract (300 mg/kg BW) was administered orally 2 days before and 8 days concurrently with gentamicin (80 mg/kg BW). Saline treated animals served as control. Estimations of urine creatinine, glucose, blood urea, serum creatinine, plasma and kidney tissue MDA were carried out after 8 days of gentamicin treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 896% and 461% respectively, with gentamicin, compared to saline treated group. Creatinine clearance was significantly decreased with gentamicin. Ginkgo biloba extract protected rats from gentamicin-induced nephrotoxicity. Changes in blood urea, serum creatinine and creatinine clearance induced by gentamicin were significantly prevented by Ginkgo biloba extract. There was a 177% and 374% rise in plasma and kidney tissue MDA with gentamicin, which were significantly reduced to normal with Ginkgo biloba extract. Histomorphology showed necrosis and desquamation of tubular epithelial cells in renal cortex with gentamicin, while it was normal and comparable to control with Ginkgo biloba extract. These data suggest that supplementation of Ginkgo biloba extract may be helpful to reduce gentamicin nephrotoxicity.

Administration, Oral↗
PubMed1991

Plasticity mechanisms in vestibular compensation in the cat are improved by an extract of Ginkgo biloba (EGb 761).

The effects of administration of an extract of Ginkgo biloba (EGb 761) on vestibular compensation was studied in unilateral vestibular neurectomized cats. This experimental model of CNS plasticity was investigated by using behavioral tests (postural disorders compensation, locomotor balance recovery), electrophysiological (spontaneous and evoked neck muscle activity) and neurophysiological (spontaneous firing rate recovery of deafferented vestibular cells) recordings, and immunocytochemical methods (synaptic loss and synaptic reoccupation within the deafferented vestibular nuclei). In all experiments, EGb 761 was administered over 30 days at daily doses of 50 mg/kg IP. The results showed a faster recovery in the EGb-treated group of cats as compared to an untreated control group. EGb administration strongly accelerated postural and locomotor balance recovery. Concomitantly, spontaneous neck muscle activity, vestibulo-collic reflexes and spontaneous firing rate of vestibular units located on the lesioned side were restored earlier. Morphological correlates characterized by a more rapid synaptic reoccupation were found in the deafferented medial vestibular nucleus by means of immunoreactive labelling using an antibody against a synaptic vesicle-associated protein (synaptophysin), but they displayed a longer time-constant in comparison with the behavioral and neurophysiological data. These results clearly demonstrate that EGb 761 acts on recovery mechanisms considered as key processes in vestibular compensation. They suggest that this substance would possess neurotrophic and/or neuritogenic properties improving functional recovery after CNS injury.

Animals↗
PubMed2002

Protective effects of Ginkgo biloba extract on rats during cerebral ischemia/reperfusion.

OBJECTIVE: To study the effect of Ginkgo biloba extract on rats during ischemia/reperfusion and its influence on intracellular calcium in hippocampal neurons. METHODS: Model of intraluminal occlusion of the middle cerebral artery (MCAO) was used to prepare the ischemia/reperfusion cortex tissue. Concentration of MDA was determined by measuring thiobarbituric acid-reactive substance. GSH-PX was quantified using the thiobarbituric acid (TBA) technique. SOD was assayed througha xanthine method. Endogenous amino acids were quantified by high performance liquid chromatographic (HPLC) analysis. Primary culturs of hippocampal neurons were prepared for a free intracellular calcium ([Ca(2+)]I) assay by Fura-2 based single cell microfluoremetric technique. RESULTS: Comparing control and treatment groups, the concentration of SOD and GSH-PX were higher, whereas that of MDA was much lower; the concentration of glutamate and aspartate decreased and that of GABA increased markedly at all time point (P < 0.01), Gly also decreased at some time points (P < 0.05). The differences were significant between the groups of 10 mg/kg, 15 mg/kg and the groups of 5 mg/kg. When 1 x 10(-5) mol/L glutamate was applied with 25 micro g/ml ginkgo biloba extract to cultured neurons, the increase in [Ca(2+)]I was lower than that caused by applying glutamate alone. Its peak value was much lower and increased phase was longer, its declining phase was shorter. After returning to baseline, the application of 1 x 10(-5) mol/L glutamate could induce the reaction to recover. CONCLUSIONS: Ginkgo biloba extract could protect damaged neurons by keeping the balance of inhibitory/excitatory aminoacids, enhancing the free radical scavengers system, and inhibiting the effect of glutamate on [Ca(2+)]I.

Amino Acids↗
PubMed2000

The effect of 3-month ingestion of Ginkgo biloba extract on pancreatic beta-cell function in response to glucose loading in normal glucose tolerant individuals.

Ginkgo biloba extract is ingested on a chronic basis for enhancing mental focus and improving cognitive function in the elderly. This study was undertaken to determine the effect of Ginkgo biloba extract on glucose-stimulated pancreatic beta-cell function in normal glucose-tolerant individuals. Twenty individuals (14 females and 6 males, ages 21-57 years) underwent a 2-hour 75 g oral glucose tolerance test (OGTT) before and after ingestion of Ginkgo biloba extract (120 mg/day at bedtime) for 3 months. Ginkgo biloba extract ingestion caused a decrease in systolic blood pressure from 125 +/- 15 to 118 +/- 12 mmHg (p < 0.05) and in diastolic blood pressure from 86 +/- 10 to 68 +/- 10 (p < 0.01). Fasting plasma insulin and C-peptide were increased, and the insulin and C-peptide areas under the curve during the OGTT changed from 136 +/- 55 to 162 +/- 94 microU/ml/h (p = 0.1232) and 9.67 +/- 5.34 to 16.88 +/- 5.20 ng/ml/h (p < 0.001), respectively. The observed dissimilar insulin/C-peptide response curves may be due to Ginkgo biloba-induced increase of the rate of insulin metabolic clearance.

Adult↗
PubMed1998

[The results of using different forms of a Ginkgo biloba extract (EGb 761) in the combined treatment of patients with circulatory encephalopathy].

Studies made in 208 patients with discirculatory encephalopathy using clinical and neuropsychological tests, apparatus (REG, ECG, EEG, Doppler sonography) and laboratory (coagulogramme) methods showed the prescription of drug preparations from ginkgo extract to be a worth-while exercise likely to benefit the patient during different stages of his/her affection. Positive time-related course was recordable of change in elastic and tonic characteristics of vessels, of bioelectric brain activity, emotional and behavioral, cognitive and mnestic features. The above-mentioned drugs will, we believe, help in developing new options for the outpatient, hospital, and rehabilitative stage of managing a patient. Potentiation of the positive action of ginkgo preparations showed up when being combined with a complex of components of the tricarboxylic acid cycle.

Adult↗
PubMed2004

Electropharmacological actions of Ginkgo biloba extract on vascular smooth and heart muscles.

Ginkgo biloba extract (GBE) is composed mostly of two constituents: One is terpenoids (such as bilobalide, ginkgolides A, B and C), and the other is flavonoids (such as quercetin and rutin). After oral administration of GBE (160 mg) to healthy volunteers, the plasma concentrations of ginkgolides A and B and bilobalide are 41.8, 5.6 and 37.6 ng/ml, respectively. GBE and bilobalide cause a potent concentration-dependent relaxation. NG-Monomethyl-l-arginine acetate (l-NMMA), an NO synthesis inhibitor, reduces the vasodilation induced by GBE. Furthermore, the vasorelaxation of GBE is attenuated in Ca2+-free medium. Bilobalide possesses similar mechanisms. The other constituents also produce vasorelaxation. On the other hand, all the compounds markedly modify the action potential configuration in guinea pig ventricular cardiomyocytes. GBE prolongs the action potential duration (APD), whereas bilobalide shortens the APD. In patch-clamp experiments, GBE markedly inhibits the Ca2+ current (ICa), the delayed rectifier K+ current (IK) and the inwardly rectifying K+ current (IK1). On the contrary bilobalide enhances the ICa and IK currents concentration-dependently. The other constituents do not cause their actions in a uniform direction. In the rat sino-atrial (SA) node, GBE causes a negative chronotropic effect. These results indicate that GBE and the constituents produce effective electropharmacological actions in the cardiomyocytes and cause vasodilation, mainly due to the inhibitions of Ca2+ influx through the Ca2+ channel and the activation of NO release in the endothelium and aortic vascular muscles.

Action Potentials↗