Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ginkgo Extract”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

[Ginkgo biloba extract and folic acid in the therapy of changes caused by autonomic neuropathy].

10 patients suffering from neuropathies caused by various diseases and with an autonomic disregulation of skin were treated intravenously with a new combination of 87.5 mg Ginkgo-biloba-extract standardized to 21.0 mg Flavonglycosids and 3 mg folic acid during 14 days. The autonomic nerve-function was measured immediately before onset and after the end of therapy with the hyperthermal laser-Doppler-Flowmetry. Additionally pain, superficial and deep sensibility were described. After the end of treatment the autonomic nerve-function was improved in a significant manner (p less than 0.01). An improvement of the described parameters for pain and for perception could be observed too. Therefore this new combination seems to be suited for treatment of polyneuropathies.

Adult↗

Phase II study with 5-fluorouracil and ginkgo biloba extract (GBE 761 ONC) in patients with pancreatic cancer.

The aim of the study was to evaluate the efficacy and tolerability of as well as the quality of life under treatment with 5-fluorouracil (CAS 51-21-8, 5-FU) combined with parenteral GBE 761 ONC (i.e. the ginkgo biloba special extract EGb 761) in patients with pancreatic cancer. Forty-eight patients with locally or metastatic advanced pancreatic cancer were treated within a phase II study. The treatment was repeated every three weeks until progression. Response to therapy was evaluated after 2 and 4 treatment courses. Thirty-two patients were evaluable for response. Progressive disease was observed in 22 (68.8%) patients, no change in 7 (21.9%) patients and partial response in 3 (9.4%) patients (overall response = 9.4%). GBE 761 ONC was well tolerated. Adverse events which occurred during the study consisted mainly of myelosuppression and gastrointestinal symptoms and were judged as 5-FU-related or consisted of liver toxicity, respectively, and were judged as tumour-related. These results suggest a good benefit-risk ratio of the combination of 5-FU and GBE 761 ONC in the treatment of pancreatic cancer. In comparison with the results of studies with either 5-FU or gemcitabine as single agents the combination of 5-FU/GBE 761 ONC shows comparable response rates. The toxicity of the 5-FU/GBE 761 ONC combination was low. This combination therapy therefore warrants further clinical investigation, such as a controlled clinical trial against 5-FU or gemcitabine monotherapy.

Adolescent↗

Extracts of Ginkgo biloba and Panax ginseng protect brain proteins from free radical induced oxidative damage in vitro.

Oxidative damage to normal human brain tissue was induced following exposure to hydroxyl (OH.) or superoxide (O2-.) free radical species generated by CO60 irradiation in vitro. Both enzymic and cytoskeletal proteins showed substantial (dose dependent) oxidative damage following exposure to OH. or O2-., as quantified by SDS-polyacrylamide gel electrophoretic analysis. Extracts of Ginkgo biloba or Panax ginseng showed a remarkable capacity to protect brain tissue proteins from oxidative damage in vitro, even at extreme (2000 kRads) dosage levels of OH. or O2-.. We suggest, therefore, that the beneficial effect of these plant extracts in preventing brain tissue damage in vivo (e.g. following ischemia-reperfusion) may result from their action in protecting brain proteins from oxidative damage, in addition to their previously reported capacity to reduce free radical induced lipid peroxidation.

Brain Damage, Chronic↗

Effects of extract of Ginkgo biloba with venlafaxine on brain injury in a rat model of depression.

BACKGROUND: Recent studies have indicated that chronic stress may give rise to brain damage, which is related to the genesis of depression. The purpose of this study is to investigate the effects of extract of Ginkgo biloba (EGb) and venlafaxine on depression. METHODS: Rats were treated with chronic and comprehensive stress to create a depression model. Immunohistochemistry was used to detect the expression of brain-derived neurotrophic factor (BDNF) in the hippocampal CA3 neurons of rats treated with different drugs. Behavioral changes of these rats were also examined. RESULTS: The expression of BDNF in the hippocampal CA3 neurons of the depression model decreased with a reduction in exploring behavior and a significant increase in fecal production. The expression of neuron nitric-oxide synthase (nNOS) protein also increased in the rats compared to normal controls. The rats treated with EGb and venlafaxine showed an increase in expression of BDNF and exploring behavior compared to untreated rats, but a decrease in nNOS and fecal production. CONCLUSIONS: Rats sustain damage to the brain after being subjected to chronic and comprehensive stress. Our research has indicated that combined EGb with venlafaxine enhances the protection of neurons and decreases damage to the brain, while relieving the side effects of synthetic antidepressants.

Animals↗

In vitro and in vivo effects of Ginkgo biloba extract EGb 761 on seeded Schwann cells within poly(DL-lactic acid-co-glycolic acid) conduits for peripheral nerve regeneration.

This study investigated the effects of Ginkgo biloba (EGb 761) extract on seeded Schwann cells within poly(DL-lactic acid-co-glycolic acid) (PLGA) conduits by in vitro and in vivo trials for peripheral nerve regeneration. The seeding efficiency of Schwann cells in serum-deprived culture medium, which simulated the environment of mechanical trauma on an injured nerve site, was improved by adding different dosages of EGb 761 (0, 1, 10, 20, 50, 100, 200 microg/mL). The analytical results showed enhanced cell attachment and survival, reduced LDH release and increased MTT values, particularly in the range 10-100 microg/mL. The PLGA nerve conduits seeded with Schwann cells (6 x 10(3) cells) and filled with gelatin containing EGb 761 (0, 10, 50, 100 microg/mL) were implanted to 10-mm right sciatic nerve defects in rats. Autograft was performed as another control. Electromyography was assessed based on the motor unit action potential (MUAP) and fibrillation potential (Fib) at 2, 4, and 6 weeks during all periods. The specimens of the experimental and control groups were harvested for histological analysis at 6 weeks after surgery. The Fib was found to gradually decay, and the MUAP was found not to be present until 4 weeks after surgery. Meanwhile, the experimental groups were all statically better than the control group (without EGb 761) and autografts were observed at 6 weeks, especially at the concentration of 10 microg/mL, where there was higher amplitude of MUAP and a significantly larger number of myelinated axons. This study concluded that a proper concentration of EGb 761 (10-50 microg/mL) promoted seeding efficiency of Schwann cells in a tissue-engineered PLGA conduit. Addition of EGb 761 in Schwann cells-seeded conduit could increase the total number of myelinated axons in nerve regeneration and improve peripheral nerve functional recovery.

Animals↗

Determination of quercetin and kaempferol in human urine after orally administrated tablet of ginkgo biloba extract by HPLC.

A sensitive, simple and accurate method was developed for determination of quercetin and kaempferol in human urine by reversed phase high performance liquid chromatography. The urine samples were analyzed on C18 column. Quercetin and kaempferol were analyzed simultaneously with good separation. UV detector was set at 380 nm. There was a linear relationship between chromatographic area of analytes and concentration of analytes over the concentration range 1.638-81.90 and 1.872-93.60 ng/ml for quercetin and kaempferol, respectively. The recovery of the assay was 99.7+/-6.2 and 97.4+/-7.2% for quercetin and kaempferol, respectively. The within-day and between-day coefficients of variation were less than 9.7 and 16.5% (RSD), respectively. The limit of detection was 1.0 ng/ml for quercetin and 1.1 ng/ml for kaempferol. The limit of quantitation was 1.61+/-0.11 ng/ml (n=5) for quercetin and 1.85+/-0.11 ng/ml (n=5) for kaempferol. The method developed has been applied to determine quercetin and kaempferol after orally administrated tablet of Ginkgo biloba extract in human urine.

Calibration↗

Comparison of the contractile effects of an extract of Ginkgo biloba and some neurotransmitters on rabbit isolated vena cava.

Dose-related contractions were elicited in strips of rabbit isolated vena cava by norepinephrine (NE, IC50 approximately equal to 2.3 X 10(-7) M), dopamine (IC50 approximately equal to 6.9 X 10(-6) M), histamine (IC50 approximately equal to 2.1 X 10(-6) M) and extract of Ginkgo biloba (Gb, IC50 approximately equal to 86 micrograms/ml). Serotonin and tyramine elicited very weak contractile effects in this preparation. Phenoxybenzamine (10(-7) M) abolished the contractions elicited by NE, and blocked the effect of Gb by about 50%. Further support is provided for the therapeutic action of Gb in cardiovascular disorders.

Animals↗

A comparison study of cerebral protection using Ginkgo biloba extract and Losartan on stroked rats.

It has been well documented that oxidative stress is involved in stroke. Currently, many neuroprotective strategies have been targeted at molecules that are able to act as an oxidant to intervene with free-radical mediated apoptosis in the ischemic penumbra. In particular, natural products which contain antioxidant properties have undoubtedly efficacious for stroke treatment. In the current study, therapeutic effects of Ginkgo biloba extract (EGb) against cerebral protection in Wistar rats underwent middle cerebral artery occlusion (MCAO) was evaluated. A comparison study was conducted by using Losartan, an antihypertensive drug. Gene expression levels of pro-apoptotic genes (AT2 receptor, Fas, Bax and Bcl-xS) have shown to have significant reduction by EGb- and Losartan-treated groups as compared to vehicle group. Significant reduction of immunoreactivity of protein production of these genes, together with least nuclear green fluorescence observed in TUNEL, EGb, as an antioxidant drug, is concluded to have potent and promising therapeutic effect for stroke treatment.

Angiotensin II Type 1 Receptor Blockers↗

Platelet-activating factor is an important mediator in hypoxic ischemic brain injury in the newborn rat. Flunarizine and Ginkgo biloba extract reduce PAF concentration in the brain.

Hypoxic-ischemic encephalopathy is still a very important cause of neonatal mortality and morbidity. Recently, platelet-activating factor (PAF) has been accused of being responsible for the neuronal damage in hypoxic-ischemic brain. We investigated tissue PAF concentrations in hypoxic-ischemic brain injury in immature rats. Endogenous PAF concentration in brain tissue showed a marked increase in hypoxic-ischemic pups (85.6 +/- 15.5 pg/mg protein) when compared to that of control (9.05 +/- 3.1 pg/mg protein). In addition, we examined the effects of flunarizine, a selective calcium channel blocker, and Ginkgo biloba extract (EGb 761) on endogenous PAF concentration in hypoxic-ischemic brain injury. Endogenous PAF concentrations in both flunarizine-pretreated (16.6 +/- 4.8 pg/mg protein) and EGb 761-pretreated (33.5 +/- 8.9 pg/mg protein) pups were significantly lower than the untreated group. These results indicate that PAF is an important mediator in immature rat model of cerebral hypoxic-ischemic injury. The suppressor effect of flunarizine and EGb 761 on PAF production may open new insight into the treatment of hypoxic-ischemic brain injury.

Animals↗

[Effect of Ginkgo biloba extract on the hemato-encephalic barrier].

The different methods used to explore the blood-brain barrier (made up of cerebral capillary vessels), and notably, at molecular level, isolated microvessel preparations, have greatly improved our knowledge in this particular field. Some of these methods could be used to evaluate the protective effects of therapeutic substances, such as Ginkgo biloba extract, on the blood-brain barrier.

Aging↗

The effect of ginkgo biloba extract on EEG spectra in experimental diabetes: no relation to lipid peroxidation.

Forty four Swiss albino rats aged two months, weighing 180-250 g, were used in the experiment. They were divided into four equal groups as control, alloxan-diabetic, diabetic + GbE and control + GbE. After the onset of experimental period, diabetic + GbE and control + GbE groups received ginkgo biloba extract and the other groups were given saline solution for ten weeks. Diabetic and diabetic + GbE groups were made diabetic by injecting alloxan on 16th day. Spectral analysis of EEGs recorded from parietal lobes of all groups of rats were computed by Fast Fourier Transform (FFT) algorithm. Their amplitude maxima were found to occupy the frequency bands of 1-2, 2-4, 4-6, 6-8, 8-16 and 16-30 Hz. Significant amplitude increase was found in 1-2 and 2-4 Hz frequency bands in diabetic + GbE group compared with control, but no differences were found for other groups.

Animals↗

Alzheimer's disease, the nematode Caenorhabditis elegans, and ginkgo biloba leaf extract.

Alzheimer's disease (AD) is affecting larger and larger proportions of our population as lifespan increases. Thus, the means to prevent or reduce the rate of this disorder is a high priority for medical research. A standardized extract of Ginkgo biloba leaves EGb 761 is a popular dietary supplement taken by the general public to enhance mental focus and by the elderly to delay onset of age-related loss of cognitive function. EGb 761 has been used for treatment of certain cerebral dysfunctions and dementias associated with aging and AD. Substantial evidence indicates that EGb 761 has neuroprotective effects. But, mechanisms of action of the components of the extract are, unfortunately, poorly understood. Research in my laboratory focuses on understanding mechanisms of action of the components of the herbal extract EGb 761 in protection against Alzheimer's disease. We have demonstrated that EGb 761 inhibited amyloid beta aggregation in vitro and attenuates reactive oxidative species (ROS) in a model organism - the round worm Caenorhabditis elegans. Furthermore, EGb 761 eased its toxicity in the transgenic C. elegans. We also found that only a certain size of the amyloid beta aggregates is toxic to the worms. These findings suggest that EGb 761 has a clear therapeutic potential for prevention and/or treatment of AD. A better understanding of the mechanisms of neuroprotection by EGb 761 will be important for designing therapeutic strategies, for basic understanding of the underlying neurodegenerative processes, and for a better understanding of the effectiveness and complexity of this herbal medicine.

Alzheimer Disease↗

A double-blind, placebo-controlled trial of extract of Ginkgo biloba added to haloperidol in treatment-resistant patients with schizophrenia.

BACKGROUND: Many studies have indicated that excess free radical formation may be involved in the pathogenesis of patients with schizophrenia. Some investigators suggested that the use of free radical scavengers might provide improvement in schizophrenia. The aim of this study was to determine the effectiveness and to evaluate the side effects of extract of Ginkgo biloba (EGb) plus haloperidol in chronic, treatment-resistant inpatients with schizophrenia. METHOD: One hundred nine patients meeting DSM-III-R criteria for schizophrenia completed a double-blind, placebo-controlled, parallel-group study of EGb plus haloperidol. Fifty-six of the patients were randomly assigned to receive a fixed dose of 360 mg/day of EGb plus a stable dose of haloperidol, 0.25 mg/kg/day, and 53 were assigned to receive placebo plus the same dose of haloperidol for 12 weeks. Patients were assessed using the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Negative Symptoms (SANS), and the Scale for the Assessment of Positive Symptoms (SAPS) at baseline, week 6, and week 12 and the Treatment Emergent Symptom Scale (TESS) for side effects at week 12. RESULTS: There was a significant reduction in both groups in BPRS total score after 12 weeks of treatment (p < .05). However, a significant reduction in total SAPS and SANS scores was noted in the EGb group (p < .05), but not in the placebo group. There was a lower SAPS total score in the EGb group than in the placebo group at the end of 12 weeks of treatment (p < .05). Of those treated with EGb plus haloperidol, 57.1% were rated as responders as compared with only 37.7% of those receiving placebo plus haloperidol when assessed by the SAPS (chi2 = 4. 111, p = .043). After 12 weeks of treatment, TESS subscore 1 (behavioral toxicity) and subscore 3 (symptoms of nerve system) were significantly decreased in the EGb group compared with the placebo group (p < .05). CONCLUSION: EGb treatment may enhance the effectiveness of antipsychotic drugs and reduce their extrapyramidal side effects.

Antipsychotic Agents↗

[Idiopathic cyclic edema. The role of capillary hyperpermeability and its correction by Ginkgo biloba extract].

Idiopathic cyclic oedema is a frequent and often unrecognized condition in young women. It is characterized by water and sodium retention with secondary hyperaldosteronism due to capillary hyperpermeability. Treatment is not easy. It includes spironolactone, sometimes sympathomimetics and hygienic-dietetic measures. Thiazide diuretics and laxatives must be avoided. Correcting the capillary defect is of paramount importance. This defect is detected and measured by Landis' labelled albumin test. The authors have tried Ginkgo biloba extract administered either orally or by intravenous infusion. Full correction of the biological anomaly was obtained in 10 cases in which Landis' test was performed before and after oral treatment, and in the 5 cases treated by intravenous infusion.

Capillary Permeability↗

Changes in zinc levels and superoxide dismutase activities in the skin of acute, ultraviolet-B-irradiated mice after treatment with ginkgo biloba extract.

Acute ultraviolet-B (UV-B) irradiation is known to act as an initiator in the formation of reactive oxygen species. These oxygen products are highly reactive and they are able to cause irreversible damage to cellular components. Oxygen free radicals are normally neutralized by very efficient systems in the body. These include antioxidant enzymes like superoxide dismutase (SOD). In a healthy subject, there is a balance between free radicals and the levels of antioxidants. In some pathological conditions such as oxidative stress, the level of antioxidants is significantly reduced. The skin contains relatively high levels of zinc (Zn), an essential element known to be a cofactor in some metabolic pathways. Zinc has also been reported to have antioxidant properties. In the present study, we investigated the effect of ginkgo biloba extract (Gbe), a potent free-radical scavenger, on UV-B-irradiated skin by measuring SOD activity and Zn levels in the skin, before and after treatment. The SOD activity was decreased after UV-B exposure, in comparison with the control group (p < 0.05). After Gbe treatment, the SOD activity increased (p < 0.05) as compared with the untreated UV-B irradiated group. The Zn levels changed in the same pattern as the SOD activity values.

Animals↗

Modification of cisplatin-induced renal p-aminohippurate uptake alteration and lipid peroxidation by thiols, Ginkgo biloba extract, deferoxamine and torbafylline.

To determine whether inhibition of lipid peroxidation modifies cisplatin-induced changes of renal p-aminohippurate (PAH) uptake, we examined the effects of various radical scavengers and torbafylline on cisplatin-induced lipid peroxidation and PAH accumulation changes in rat renal cortical slices. Renal cortical slices were incubated with different cisplatin concentrations (0.3, 0.6, 1.0 mg/ml) in the presence of either glutathione, N-acetylcysteine, the iron chelator deferoxamine, Ginkgo biloba extract or the xanthine derivate torbafylline. Lipid peroxidation monitored as the production of malondialdehyde (MDA) was stimulated by increasing cisplatin concentrations in a dose-related manner. At a cisplatin concentration of 1.0 mg/ml, MDA production was twofold compared to controls (0.69 +/- 0.06 vs. 1.36 +/- 0.07 nmol/mg; p < 0.05). In turn, cisplatin decreased PAH uptake of kidney slices dose-dependently from 13.3 +/- 1.3 to 2.6 +/- 0.2 (p < 0.01). All agents tested inhibited cisplatin-induced lipid peroxidation; however, at a cisplatin concentration of 1.0 mg/ml, none of them prevented the decline of cisplatin-induced PAH uptake. Of the agents tested, deferoxamine proved to be the most effective antioxidant, completely inhibiting cisplatin-induced lipid peroxidation but in contrast preventing the decrease in PAH uptake only at a cisplatin concentration of 0.3 mg/ml. No strict association between lipid peroxidation and decline of PAH uptake was found, suggesting that lipid peroxidation may only in part participate in cisplatin-induced alterations of PAH uptake.

Acetylcysteine↗