Search results for "Ginkgo"

showing 10 items of 21 documents

Optimization of fermentation parameters with magnetically immobilized Bacillus natto on Ginkgo seeds and evaluation of bioactivity and safety

2018

Abstract In this study, magnetically immobilized Bacillus natto fermentation approach was developed on Ginkgo seeds. Some parameters potentially influencing the fibrinolytic activity of fermented Ginkgo seeds were systematically investigated and optimized by Plackett-Burman and Box-Behnken designs, and the optimum fermentation conditions obtained were 60 mesh particle size, 150 rpm stirring rate, fermentation pH 6.5, 43.0 h fermentation time, 36.4 °C temperature, 16.4 mL/g liquid-solid ratio and 1.0 g/g beads-solid ratio. After fermentation, the satisfactory fibrinolytic activity of Ginkgo seeds was 3175 ± 43 IU/g. The total flavonoid contents were reached to 2.6 ± 0.2 mg rutin equivalent/g…

0106 biological scienceschemistry.chemical_classificationbiologyBacillus nattoGinkgoMicroorganismFlavonoidfood and beverages04 agricultural and veterinary sciencesbiology.organism_classification040401 food science01 natural sciencesRutinchemistry.chemical_compound0404 agricultural biotechnologychemistryUntreated control010608 biotechnologyFermentationFood scienceFood ScienceLWT
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Ginkgo biloba induces different gene expression signatures and oncogenic pathways in malignant and non-malignant cells of the liver

2018

Ginkgo biloba (EGb761) is a widely used botanical drug. Several reports indicate that EGb761 confers preventive as well as anti-tumorigenic properties in a variety of tumors, including hepatocellular carcinoma (HCC). We here evaluate functional effects and molecular alterations induced by EGb761 in hepatoma cells and non-malignant hepatocytes. Hepatoma cell lines, primary human HCC cells and immortalized human hepatocytes (IH) were exposed to various concentrations (0-1000 μg/ml) of EGb761. Apoptosis and proliferation were evaluated after 72h of EGb761 exposure. Response to oxidative stress, tumorigenic properties and molecular changes were further investigated. While anti-oxidant effects w…

0301 basic medicineCarcinogenesisApoptosismedicine.disease_causeBiochemistryAntioxidantsTranscriptome0302 clinical medicineCell SignalingAnimal CellsMedicine and Health SciencesCellular Stress ResponsesCultured Tumor CellsMultidisciplinaryCell DeathbiologyGinkgo bilobaTOR Serine-Threonine KinasesLiver NeoplasmsQRLiverOncologyCell Processes030220 oncology & carcinogenesisHepatocellular carcinomaMedicineBiological CulturesCellular TypesAnatomyResearch ArticleSignal TransductionCarcinoma HepatocellularNF-E2-Related Factor 2ScienceResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineHumansCell ProliferationOncogenic SignalingPlant ExtractsBiology and Life SciencesGinkgo bilobaCell BiologyCell Culturesbiology.organism_classificationmedicine.diseaseOxidative Stress030104 developmental biologyCell cultureApoptosisCancer cellHepatocytesCancer researchHepatoma CellsTranscriptomeCarcinogenesisOxidative stressPLOS ONE
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ADAM10 in Alzheimer's disease: Pharmacological modulation by natural compounds and its role as a peripheral marker.

2019

Abstract Alzheimer’s disease (AD) represents a global burden in the economics of healthcare systems. Amyloid-β (Aβ) peptides are formed by amyloid-β precursor protein (AβPP) cleavage, which can be processed by two pathways. The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques. This pathway remains largely unknown and ignored, mainly regarding pharmacological approaches that may act via different signaling cascades and thus stimulate non-amyloidogenic cleavage through ADAM10. This review emphasizes the effects of natural compounds on ADAM10 modulation, which eventuates in a neuroprotective mechanism. M…

0301 basic medicineFarmacologiaADAM10DiseaseRM1-950Natural compoundsCleavage (embryo)NeuroprotectionCatechin03 medical and health sciencesADAM10 ProteinAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseDisintegrinHumansSenile plaquesPharmacological modulationPharmacologyMetalloproteinaseAmyloid beta-PeptidesbiologyChemistryPlant ExtractsADAM10ProteinsGinkgo bilobaMembrane ProteinsGeneral Medicineα-SecretaseAlzheimer's disease030104 developmental biologyMalaltia d'AlzheimerNeuroprotective Agents030220 oncology & carcinogenesisPharmaceuticalbiology.proteinTherapeutics. PharmacologyAmyloid Precursor Protein SecretasesNeuroscienceAlzheimer’s diseaseProteïnesBiomarkersBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Excitotoxic Hippocampal Membrane Breakdown and its Inhibition by Bilobalide: Role of Chloride Fluxes

2003

We have previously shown that hypoxia and N-methyl-D-aspartate (NMDA) receptor activation induce breakdown of choline-containing phospholipids in rat hippocampus, a process which is mediated by calcium influx and phospholipase A (2) activation. Bilobalide, a constituent of Ginkgo biloba, inhibited this process in a potent manner (Weichel et al., Naunyn-Schmiedeberg's Arch. Pharmacol. 360, 609-615, 1999). In this study, we used fluorescence microscopy and radioactive flux measurements to show that bilobalide does not interfere with NMDA-induced calcium influx. Instead, bilobalide seems to inhibit NMDA-induced fluxes of chloride ions through ligand-operated chloride channels. In our experimen…

Calcium IsotopesMaleN-Methylaspartatemedicine.drug_classGlycineCyclopentanes44'-Diisothiocyanostilbene-22'-Disulfonic AcidIn Vitro TechniquesHippocampusChlorideCholinechemistry.chemical_compoundChloridesBilobalideFurosemideExcitatory Amino Acid AgonistsmedicineAnimalsCholineDrug InteractionsPharmacology (medical)Channel blockerRats WistarDiureticsFuransCell MembraneGeneral MedicineReceptor antagonistPyrrolidinonesRatsPsychiatry and Mental healthGinkgolidesnervous systemchemistryBiochemistryDIDSPotassiumChloride channelBiophysicsNMDA receptorCalciumDiterpenesDizocilpine MaleateExcitatory Amino Acid AntagonistsSynaptosomesmedicine.drugPharmacopsychiatry
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Neuroprotective potential of Ginkgo biloba in retinal diseases

2019

AbstractLike other tissues of the central nervous system, the retina is susceptible to damage by oxidative processes that result in several neurodegenerative disease such as age-related macular degeneration, diabetic retinopathy, glaucoma, ischaemic retinal disease, retinal disease produced by light oxidation, and detached retina, among other diseases. The use of antioxidant substances is a solution to some health problems caused by oxidative stress, because they regulate redox homeostasis and reduce oxidative stress. This is important for neurodegeneration linked to oxidation processes. In line with this, Ginkgo biloba is a medicinal plant with excellent antioxidant properties whose effect…

Ginkgo biloba - Uso terapéutico.Pharmaceutical SciencePharmacologymedicine.disease_cause01 natural sciencesNeuroprotectionAnalytical Chemistrychemistry.chemical_compoundRetinal DiseasesGinkgo biloba - Therapeutic use.Drug DiscoveryAnimalsHumansMedicinePharmacologyRetinabiologyPlant Extracts010405 organic chemistrybusiness.industryGinkgo bilobaRetina - Diseases - Treatment.System nervous - Degeneration - Treatment.Organic ChemistryNeurodegenerationGinkgo bilobaNeurodegenerative DiseasesRetinalDiabetic retinopathyMacular degenerationmedicine.diseasebiology.organism_classificationEye - Diseases - Treatment.0104 chemical sciencesSistema nervioso - Degeneración - Tratamiento.010404 medicinal & biomolecular chemistryNeuroprotective Agentsmedicine.anatomical_structureComplementary and alternative medicinechemistryOjos - Enfermedades - Tratamiento.Molecular MedicinebusinessOxidative stressPhytotherapyRetina - Enfermedades - Tratamiento.
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Effect of the extract of Ginkgo biloba (EGb 761) on the circulating and cellular profiles of polyunsaturated fatty acids: correlation with the anti-o…

2000

Abstract Ginkgo biloba extract (EGb 761) has beneficial effects on cognitive functions in aging patients, and on various pathologies, including cardiovascular diseases. Although the extract is known to have antioxidant properties and improve membrane fluidity, the cellular mechanisms underlying these effects have not been determined. Here, we examined the in vivo effects of EGb 761 on circulating and cellular lipids. EGb 761 treatment induced significant increases in the levels of circulating polyunsaturated fatty acids (PUFAs), and a decrease in the saturation index SI (saturated/polyunsaturated species). Plasma triglycerides and cholesterol were not affected, while phospholipids were slig…

MaleChromatography GasErythrocytesAntioxidantmedicine.medical_treatmentClinical BiochemistryPharmacologymedicine.disease_causeAntioxidantschemistry.chemical_compoundmedicineMembrane fluidityAnimalsGinkgoalesRats WistarPhospholipidsTriglycerideschemistry.chemical_classificationPlants MedicinalbiologyPlant ExtractsGinkgo bilobaCholesterolCell MembraneErythrocyte MembraneFatty AcidsGinkgo bilobaHydrogen PeroxideCell Biologybiology.organism_classificationEicosapentaenoic acidRatsOxidative StressCholesterolEicosapentaenoic AcidchemistryBiochemistryFatty Acids Unsaturatedlipids (amino acids peptides and proteins)Oxidative stressPolyunsaturated fatty acidProstaglandins, Leukotrienes and Essential Fatty Acids (PLEFA)
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Phospholipid breakdown and choline release under hypoxic conditions: inhibition by bilobalide, a constituent of Ginkgo biloba

1997

A marked increase of choline release from rat hippocampal slices was observed when the slices were superfused with oxygen-free buffer, indicating hypoxia-induced hydrolysis of choline-containing phospholipids. This increase of choline release was suppressed by bilobalide, an ingredient of Ginkgo biloba, but not by a mixture of ginkgolides. The EC50 value for bilobalide was 0.38 microM. In ex vivo experiments, bilobalide also inhibited hypoxia-induced choline release when given p.o. in doses of 2-20 mg/kg 1 h prior to slice preparation. The half-maximum effect was observed with 6 mg/kg bilobalide. A similar effect was noted after p.o. administration of 200 mg/kg EGb 761, a ginkgo extract con…

MaleDrug Evaluation PreclinicalCyclopentanesPharmacologyHippocampusCholinechemistry.chemical_compoundSlice preparationBilobalideAnimalsCholineRats WistarGinkgolidesFuransHypoxia BrainMolecular BiologyPhospholipidsEC50biologyPlant ExtractsGinkgo bilobaGeneral NeuroscienceGinkgobiology.organism_classificationRatsPlant LeavesGinkgolidesLogistic ModelschemistryBiochemistryNeurology (clinical)DiterpenesEx vivoDevelopmental BiologyBrain Research
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Bilobalide, a constituent of Ginkgo biloba , inhibits NMDA-induced phospholipase A 2 activation and phospholipid breakdown in rat hippocampus

2000

In rat hippocampal slices superfused with magnesium-free buffer, glutamate (1 mM) caused the release of large amounts of choline due to phospholipid breakdown. This phenomenon was mimicked by N-methyl-D-aspartate (NMDA) in a calcium-sensitive manner and was blocked by NMDA receptor antagonists such as MK-801 and 7-chlorokynurenate. The NMDA-induced release of choline was not caused by activation of phospholipase D but was mediated by phospholipase A2 (PLA2) activation as the release of choline was accompanied by the formation of lyso-phosphatidylcholine (lyso-PC) and glycerophospho-choline (GPCh) and was blocked by 5-[2-(2-carboxyethyl)-4-dodecanoyl-3,5-dimethylpyrrol-1-yl]pentano ic acid, …

MaleMicrodialysisN-MethylaspartateMicrodialysisGlycineCyclopentanesPharmacologyHippocampal formationHippocampusReceptors N-Methyl-D-AspartatePhospholipases ACholinechemistry.chemical_compoundPhospholipase A2BilobalideSeizuresAnimalsCholineRats WistarFuransCells CulturedPhospholipidsPharmacologyPlants MedicinalDose-Response Relationship DrugbiologyPhospholipase DGlutamate receptorGinkgo bilobaLysophosphatidylcholinesGeneral MedicineGlycerylphosphorylcholineRatsEnzyme ActivationPhospholipases A2Ginkgolideschemistrybiology.proteinNMDA receptorDiterpenesNaunyn-Schmiedeberg's Archives of Pharmacology
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Role of GABAergic antagonism in the neuroprotective effects of bilobalide

2006

Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to block GABA(A) receptors. The goal of this study was to test the potential role of a GABAergic mechanism for the neuroprotective activity of bilobalide. In rat hippocampal slices exposed to NMDA, release of choline indicates breakdown of membrane phospholipids. NMDA-induced choline release was almost completely blocked in the presence of bilobalide (10 microM) and under low-chloride conditions. Bicuculline (100 microM), a competitive antagonist at GABA(A) receptors, reduced NMDA-induced choline release to a small extent (-23%). GABA (100 microM) partiall…

MaleN-MethylaspartateBrain EdemaCyclopentanesIn Vitro TechniquesPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusArticlegamma-Aminobutyric acidCholineGABA AntagonistsRats Sprague-Dawleychemistry.chemical_compoundBilobalideExcitatory Amino Acid AgonistsmedicineAnimalsPicrotoxinDrug InteractionsFuransMolecular Biologygamma-Aminobutyric AcidChemistryGABAA receptorGeneral NeuroscienceBicucullineGABA receptor antagonistBridged Bicyclo Compounds HeterocyclicRatsGinkgolidesNeuroprotective Agentsnervous systemNonlinear DynamicsMechanism of actionArea Under CurveGABAergicNeurology (clinical)medicine.symptomSynaptosomesDevelopmental Biologymedicine.drugBrain Research
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Why Women Have More Alzheimer's Disease Than Men: Gender and Mitochondrial Toxicity of Amyloid-β Peptide

2010

The main risk factors for developing Alzheimer's disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men. Thus, there must be a specific pathogenic mechanism to explain the higher incidence of AD cases in women. In this regard, it is notable that mitochondria from young females are protected against amyloid-beta toxicity, generate less reactive oxygen species, and release less apoptogenic signals than those from males. However, all this advantage is lost in mitochondria from old females. Since estrogenic compounds protect against mitochondrial toxicity of amyloid-beta, estr…

MalePhysiologyDiseaseMitochondrionPharmacologyModels BiologicalAlzheimer DiseaseRisk FactorsmedicineHumansSex CharacteristicsAmyloid beta-PeptidesbiologyGinkgo bilobaGeneral NeuroscienceIncidence (epidemiology)EstrogensGeneral Medicinebiology.organism_classificationmedicine.diseaseMitochondriaUp-RegulationClinical trialPsychiatry and Mental healthClinical PsychologyMitochondrial toxicityToxicityFemaleGeriatrics and GerontologySex characteristicsJournal of Alzheimer's Disease
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