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PubMed2006

Paradoxical effects of ginkgolide B on cardiomyocyte contractile function in normal and high-glucose environments.

AIM: Ginkgo biloba extract is a natural product used widely for cerebral and cardiovascular diseases. It is mainly composed of terpene lactones (ginkgolide A and B) and flavone glycosides (eg quercetin and kaempferol). To better understand the cardiac electromechanical action of Ginkgo biloba extract in normal and diabetic states, this study was designed to examine the effect of ginkgolide B on cardiomyocyte contractile function under normal and high-glucose environments. METHODS: Isolated adult rat ventricular myocytes were cultured for 6 h in a serum-free medium containing either normal (NG; 5.5 mmol/L) or high (HG; 25.5 mmol/L) glucose with or without ginkgolide B (0.5-2.0 microg/mL). Mechanical properties were evaluated using the IonOptix MyoCam system. Contractile properties analyzed included peak shortening (PS), maximal velocity of shortening/relengthening (+/-dl/dt), time-to-PS (TPS) and time-to-90% relengthening (TR90). Levels of essential Ca(2+) regulatory proteins sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a), phospholamban (PLB) and Na(+)-Ca(2+) exchanger (NCX) were assessed by Western blotting. RESULTS: Ginkgolide B nullified HG-induced prolongation in TR90. However, ginkgolide B depressed PS, +/-dl/dt and shortened TPS in NG and HG cells. Ginkgolide B also prolonged TR90 in NG cells. Western blot analysis revealed that HG upregulated SERCA2a and downregulated PLB expression without affecting that of NCX. Ginkgolide B disrupted the NG-HG response pattern in SERCA2a and NCX without affecting that of PLB. CONCLUSION: Ginkgolide B affects cardiomyocyte contractile function under NG or HG environments in a paradoxical manner, which may be attributed to uneven action on Ca(2+) regulatory proteins under NG and HG conditions.

Animals↗
PubMed1995

Blockade of lithium chloride-induced conditioned place aversion as a test for antiemetic agents: comparison of metoclopramide with combined extracts of Zingiber officinale and Ginkgo biloba.

The present study tests the hypothesis that the blockade of lithium chloride-induced conditioned place aversion might be a suitable model to assess antiemetic properties of drugs, especially in species that do not vomit, like rats. The effects of the known antiemetic compound metoclopramide were compared with those of zingicomb, a combination preparation of extracts of Ginkgo biloba and Zingiber officinale, also presumed to have antiemetic properties. Place conditioning was performed using a conventional three-compartment test procedure. On three successive conditioning trials, rats received an intraperitoneal (i.p.) injection of lithium chloride (125 mg/kg) and were placed into the compartment that they had preferred over three baseline trials. During the test, rats treated with lithium chloride (LiCl) spent less time in the treatment compartment, indicative of a conditioned place aversion (CPA). In the first experiment, metoclopramide (MCP) was administered intragastrically (IG) in doses of 2 or 10 mg/kg 60 min prior to LiCl injection. The pretreatment with 50 and 100 mg/kg zingicomb attenuated the LiCl-produced CPA, whereas a dosage of 10 mg/kg had no effect. These findings suggest that LiCl-induced CPA is a viable procedure with which to assess the antiemetic properties of metoclopramide. Furthermore, the data confirm the hypothesis that the phytopharmacon zingicomb might have antiemetic properties that are comparable to those of metoclopramide.

Animals↗
PubMed2003

Behavioral effects of Ginkgo biloba L., Panax ginseng C.A. Mey. and Gincosan.

The behavioral effects of a standardized extract from Panax ginseng roots (G115), of a standardized extract from Ginkgo biloba leaves (GK501) and of their combination (PHL-00701) (Gincosan) were examined in experiments on rats with undisturbed memory and on rats with experimentally-impaired memory (by alcohol or by muscarinic- and dopamine-receptor antagonists), using methods for active avoidance (shuttle-box) and passive avoidance (step-down and step-through). On multiple administration G115, GK501 and PHL-00701 exerted favorable effects on learning and memory. These effects varied with the dose and administration schedules, with the rat strain and with the behavioral method. Based on earlier results, we discuss the role of changes in brain biogenic amines induced by the extracts in their mechanism of action. The present results allow for ranking G115, GK501 and their combination PHL-00701 (Gincosan) among cognition-enhancing (nootropic) drugs.

Animals↗
PubMed2005

Ginkgolide B, a constituent of Ginkgo biloba, facilitates glutamate exocytosis from rat hippocampal nerve terminals.

Although previous studies have demonstrated that Ginkgo biloba extract has modest effects in the improvement of memory and cognitive function of the Alzheimer's disease patients, the mechanism(s) underlying its beneficial effects remain(s) unclear. In this study, the effect of ginkgolide B, one of the major constituents of Ginkgo biloba extract, on the release of endogenous glutamate from rat hippocampal nerve terminals (synaptosomes) was studied. Ginkgolide B facilitated the Ca2+-dependent release of glutamate evoked by 4-aminopyridine in a concentration-dependent manner. The facilitatory action of ginkgolide B was not due to it increasing synaptosomal excitability because ginkgolide B did not alter the 4-aminopyridine-evoked depolarization of the synaptosomal plasma membrane potential. Rather, examination of the effect of ginkgolide B on cytosolic free Ca2+ concentration revealed that the facilitation of glutamate release could be attributed to an enhancement of presynaptic voltage-dependent Ca2+ influx. Consistent with this, the ginkgolide B-mediated facilitation of glutamate release was significantly prevented in synaptosomes pretreated with a wide spectrum blocker of N-, P-, and Q-type Ca2+ channels, omega-conotoxin MVIIC. Moreover, the facilitation produced by ginkgolide B was completely abolished by the protein kinase A inhibitor, but not by the protein kinase C inhibitor. These results suggest that ginkgolide B effects a increase in protein kinase A activation, which subsequently enhances the Ca2+ entry through voltage-dependent N- and P/Q-type Ca2+ channels to cause a increase in evoked glutamate release from rat hippocampal nerve terminals. In addition, glutamate release elicited by Ca2+ ionophore (ionomycin) was also facilitated by ginkgolide B, which suggests that ginkgolide B may have a direct effect on the secretory apparatus downstream of Ca2+ entry. These actions of ginkgolide B may provide some information regarding the beneficial effects of Ginkgo biloba in the central nervous system.

4-Aminopyridine↗
PubMed1993

Memory effects of standardized extracts of Panax ginseng (G115), Ginkgo biloba (GK 501) and their combination Gincosan (PHL-00701).

In experiments on young (aged 3 months) and old (aged 26 months) rats, using some conditioned-reflex methods with punishment or positive reinforcement for active and passive avoidance (shuttle-box, step-down, step-through, and water maze), we studied the effects of the standardized extracts of Panax ginseng (G115), Ginkgo biloba (GK501) and their combination Gincosan (PHL-00701). The extracts were administered orally for 7 days before training at three increasing doses: 17, 50, and 150 mg/kg for G115; 10, 30, and 90 mg/kg for GK501; and 27, 80, and 240 mg/kg for PHL-00701. The two extracts and their combination improved the retention of learned behavior. This effect varied considerably with the extracts, with the dose and with the behavioral method used. The results suggest that the Panax ginseng G115 and the Ginkgo biloba GK501 extracts possess properties similar in every respect to those of nootropic drugs. The favorable effects on learning and memory of the combination of G115 plus GK501 and the other pharmacological activities inherent in the extracts characterize this combination, offered as Gincosan as a particularly promising drug in geriatric practice.

Aging↗
PubMed2001

Effectiveness of Ginkgo biloba in treating tinnitus: double blind, placebo controlled trial.

OBJECTIVE: To determine whether Ginkgo biloba is effective in treating tinnitus. DESIGN: Double blind, placebo controlled trial using postal questionnaires. PARTICIPANTS: 1121 healthy people aged between 18 and 70 years with tinnitus that was comparatively stable; 978 participants were matched (489 pairs). INTERVENTION: 12 weeks' treatment with either 50 mg Ginkgo biloba extract LI 1370 three times daily or placebo. MAIN OUTCOME MEASURES: Participants' assessment of tinnitus before, during, and after treatment. Questionnaires included items assessing perception of how loud and how troublesome tinnitus was. Changes in loudness were rated on a six point scale. Changes in how troublesome were rated on a five point scale. RESULTS: There were no significant differences in primary or secondary outcome measures between the groups. 34 of 360 participants receiving active treatment reported that their tinnitus was less troublesome after 12 weeks of treatment compared with 35 of 360 participants who took placebo. CONCLUSIONS: 50 mg Ginkgo biloba extract LI 1370 given 3 times daily for 12 weeks is no more effective than placebo in treating tinnitus.

Adolescent↗
PubMed2001

Effect of biflavones of Ginkgo biloba against UVB-induced cytotoxicity in vitro.

The effect of Ginkgo biloba extract on Ultraviolet B (UVB) irradiated fibroblasts was examined by using a neutral red dye uptake assay and a lactic dehydrogenase (LDH) release assay. Crude extract along with individual components, including flavone-glycosides and biflavones, were applied to cultured normal human skin fibroblasts for 12 hours, and 0, 20, 40 and 80 mJ/cm2 of UVB were irradiated. Two synthetic flavonoids, quercetin and rutin, which have polyphenol structures close to the flavonoids in Ginkgo biloba extract, were used to compare any structure-related activity under the same conditions. At the concentrations (from 0.25 to 2 mg/ml) treated with biflavone components (isoginkgetin/ginkgetin, sciadopitysin) and quercetin, high neutral red dye uptake was detected with gradual increases in UVB irradiation. The time-course release of LDH was determined as the cytotoxicity index (%) during 24 hours following a high dose UVB irradiation (200 mJ/cm2), and the pattern of this cytotoxicity index was similar to that of the neutral red dye uptake results. Sciadopitysin, isoginkgetin/ginkgetin and quercetin treatments lowered cytotoxicity indices to 50.81, 67.81 and 62.19%, respectively, compared to 95.38% for the untreated control. The antioxidant potential of biflavones of Ginkgo biloba could be explained on the basis of structure-related activity; hydroxy- and methyl-substitutions on the basic structure of these flavonoids played a role, as other reports have suggested.

Cell Death↗
PubMedDate not supplied

Experimental retinopathy of prematurity: angiostatic inhibition by nimodipine, ginkgo-biloba, and dipyridamole, and response to different growth factors.

PURPOSE: To investigate whether commonly used vasodilating drugs ameliorate angiogenesis in experimental retinopathy of prematurity (ROP), and to study the response of these drugs to different growth factors. METHODS: We used a rat and mouse model of oxygen-induced ischemic retinopathy. Animals were treated with nimodipine, gingko-biloba and dipyridamole intraperitoneally starting the day before exposure to room air (day 1). Controls were injected with vehicle solution only. Eyes were processed histopathologically with serial sections and neovascularization was measured by counting the nuclei within the retinal internal limiting membrane, by a masked observer. Retinal and vitreous tissues were assayed by ELISA for VEGF, PDGF and TGFbeta2. RESULTS: Nimodipine significantly inhibited the growth of new vessels in rats. The number of nuclei was 310 +/- 69 in the control group (n:14) and 121 +/- 53 in the treated ones (n:14), (p<0.0005). Similar results were found with ginkgo-biloba extracts: 344 +/- 53 (n:15) in controls, and 136 +/- 29 (n:11) in treated ones (p<0.0005), and with dipyridamole: 303 +/- 69 (n:13) in controls, and 131 +/- 48.5 in treated rats (p<0.0005). Results were similar in mice. 186 +/- 45 (n:7) nuclei counted in controls against 90 +/- 25 (n:6) for dipyridamole treated (p<0.0005); and 81 +/- 21 for ginkgo-biloba treated animals (p<0.0005). A gradual, very significant increase in VEGF values in response to relative hypoxia (room air) contrasted with the significant inhibition noted both with ginkgo-biloba extracts and dipyridamole. TGFbeta2 and PDGF both showed a gradual increase in relative hypoxia at days 2 and 4 of room air (p<0.0005). Treated animals showed marked inhibition of the three growth factors. CONCLUSIONS: All three drugs markedly inhibited angiogenesis in experimental ROP. Growth factors were elevated in hypoxic conditions. Treated animals showed significant decreases of PDGF, VEGF, and TGFbeta2 in retinal and vitreous tissues.

Animals↗
PubMed1996

Hypoxia-dependent changes of enzyme activities in different fibre types of rat soleus and extensor digitorum longus muscles. A cytophotometrical study.

Using cytophotometry activity changes of succinate dehydrogenase, glycerol-3-phosphate dehydrogenase and myofibrillar adenosine triphosphatase were measured in 3 fibre types of soleus and extensor digitorum longus muscles under normal and experimental conditions. Fibres were typed by means of cytophotometrical data into slow-oxidative, fast-oxidative glycolytic and fast-glycolytic ones. After experimental hypoxia of 20 min duration a significant increase of enzyme activities was observed especially in slow-oxidative and fast-oxidative glycolytic fibres of both muscles, e.g. succinate dehydrogenase activity increased by 21% in these fibres of soleus muscle and by 23-26% in these fibres of extensor digitorum longus muscle. Moreover, an increase of glycerol-3-phosphate dehydrogenase activity by 10% in slow-oxidative fibres and by 28% in fast-oxidative glycolytic fibres and a 10-12% increased ATPase activity in all fibres of extensor digitorum longus muscle were measured. Treatment with Ginkgo biloba extract for 3 months before exposure to hypoxia resulted in increased adenosine triphosphatase activity in all fibres of both muscles and in decreased succinate dehydrogenase activity of slow-oxidative and fast-oxidative glycolytic fibres of extensor digitorum longus muscle. These results could be interpreted as a protective effect of Ginkgo biloba extract.

Adenosine Triphosphatases↗
PubMed1998

Phospholipase Cgamma1 inhibitory principles from the sarcotestas of Ginkgo biloba.

Ten phenolic compounds were isolated from the CHCl3 extract of Ginkgo biloba sarcotestas (Ginkgoaceae) as a new class of phosphatidylinositol-specific phospholipase Cgamma1 (PI-PLCgamma1) inhibitors. The substances without the long chain were ineffective. On the other hand, the activities of these compounds were dramatically decreased by acetylation of aromatic hydroxyl groups of cardanol, phenolic acid, and bilobol and by methylation of the aromatic carboxyl group of phenolic acid. The unsaturated long chain as well as the aromatic hydroxyl and carboxyl groups might play a key role for the PI-PLCgamma1 inhibitory activity. These compounds also inhibited the growth of a number of human cancer cell lines, but were less cytotoxic against a human normal colon cell line.

Cells, Cultured↗
PubMed2001

Ginkgo biloba neuroprotection: Therapeutic implications in Alzheimer's disease.

An extract of Ginkgo biloba leaves, EGb761, is becoming one of the most popular dietary supplements in the United States to enhance memory. In Europe it is a commonly prescribed drug for treatment of age-related deterioration, including degenerative dementias of the Alzheimer type (AD). Substantial experimental evidence indicates that EGb761 has neuroprotective potency under conditions such as ischemia, seizures and peripheral nerve damage. However, the mechanisms of such neuroprotective effects remain unknown, partially because of the complex chemical composition of EGb761 and the resulting so-called "polyvalent" action. This review focuses on cellular and molecular approaches towards understanding the polyvalent action of EGb761 neuroprotective effect. Two potential mechanisms of action, reducing oxidative damage and stimulating cell survival machinery, are discussed. Better understanding of the neuroprotective mechanisms of EGb761 will provide impetus for possible combination therapies and for the design of rational, "mechanism-based" strategies that target age-related neurodegeneration and Alzheimer's disease.

Journal Article↗
PubMed2005

Protective effects of different antioxidants and amrinone on vancomycin-induced nephrotoxicity.

We have studied the effects of three antioxidants and amrinone, an inotropic agent, against vancomycin-induced nephrotoxicity in rats by investigating renal function and morphology. Thirty adult female Sprague Dawley rats (168-234 g) were divided into six groups. A saline-treated group served as control. The other five groups were treated for 7 days with vancomycin alone or in combination with alpha-lipoic acid, Ginkgo biloba extract 761, melatonin or amrinone. On day 8, all the rats were sacrificed by decapitation, kidney tissues were excised immediately and blood and kidney samples were collected. Blood urea and creatinine, kidney tissue malondialdehyde levels, and kidney superoxide dismutase and glutathione (GSH) peroxidase activities were measured. The kidneys were also examined for histological changes. Vancomycin administration led to increased urea, creatinine and malondialdehyde levels and decreased superoxide dismutase and GSH peroxidase activities. Co-administration of alpha-lipoic acid, Ginkgo biloba extract, melatonin or amrinone with vancomycin prevented the increases in the urea, creatinine and melondialdehyde levels and also resulted in higher superoxide dismutase and GSH peroxidase activities. The antioxidants and AMR improved the renal pathology compared to rats treated with vancomycin alone (P<0.05). These results indicate that the three antioxidants and amrinone have potential protective effects against vancomycin-induced nephrotoxicity, which might in part be due to inhibition of free oxygen radical production. Amrinone was the most effective drug as judged on the basis of the pathological findings.

Amrinone↗
PubMed1989

[Edematous syndromes caused by capillary hyperpermeability. Diffuse angioedema].

Edema due to increased capillary permeability (ICP) may be diffuse or localized. Local edemas (Quincke edema, angioneurotic edema) are most often allergic or very rarely due to a defect in C1-inhibitor. Generalized edemas due to ICP share the following clinical features: Fluid retention (subcutaneous edema and diffused swelling) is predominant in lower limbs; it is worsened by orthostatism and warmth and alleviated by decubitus and cold, with important weight variations between morning and evening. It is associated with enhanced thirst, hypotension, oliguria, headaches and blood volume reduction; secondary hyperaldosteronism is the main mechanism. These troubles are due to ICP, associated with lymphatic drainage abnormalities; ICP is measured by the isotopic Landis Test. This abnormality is present in several diseases. Idiopathic orthostatic edema (IOE) is frequent and often unrecognized, occurring mainly in women, often associated with luteal insufficiency. Iatrogenic complications (diuretic and laxative abuses) are frequently superimposed. ICP may be corrected by vitamins P (rutin, anthocyanosides, diosmin, Ginkgo biloba extracts...) Cyclic shock due to ICP is rare. It is characterized by cyclic edema and shock with hypovolemia, hypoproteinemia; the mechanism of shock is a severe loss of fluid and protein from the vascular bed. It is often associated with monoclonal gammapathy and complement activation. In our personal case, the trouble in CP was present all along the disease with permanent edema and low blood pressure (especially in orthostatism). Vit "P" and Ginkgo biloba extracts were able to partially improve CP and the clinical troubles. However, in spite of this treatment a fatal shock occurred after ten years follow-up. Episodic angioedema associated with eosinophilia was first described by Gleich.(ABSTRACT TRUNCATED AT 250 WORDS)

Capillary Permeability↗
PubMed1999

Additional information to the in vitro antioxidant activity of Ginkgo biloba L.

The in vitro antioxidant and free radical scavenging activity of the ethanol extract from Ginkgo biloba L. was examined in different systems. The extract showed hydrogen-donating ability, reducing power, copper-binding property, free radical scavenging activity in a H2O2/.OH-luminol system and it could prevent the autoxidation of linoleic acid. All these properties are involved in the overall antioxidant activity of Ginkgo biloba which makes it suitable for the prevention of human disease in which free radicals play an important role.

Antioxidants↗
PubMed2006

Protective effects of ginkgo biloba against acetaminophen-induced toxicity in mice.

BACKGROUND: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. OBJECTIVE: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. METHODS: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. Serum ALT, AST, and tumor necrosis factor-alpha (TNF-alpha) levels in blood and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and collagen contents in liver tissues were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. RESULTS: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). CONCLUSION: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a "tissue injury-limiting agent" must be further elucidated in drug-induced oxidative damage.

Acetaminophen↗
PubMed1998

The glutathione content of retinal Müller (glial) cells: the effects of aging and of application of free-radical scavengers.

The dependence of intracellular glutathione (GSH), an important radical scavenger, on aging with or without externally applied Ginkgo biloba extract EGb 761, another established radical scavenger, was studied in guinea pig M¿ller (retinal glial) cells by using the fluorescent dye monochlorobimane. The GSH content of freshly dissociated cells from untreated aged animals was significantly lower than that of young controls; most of this reduction was prevented by application of EGb 761. Culturing the cells in amino-acid-free caused a loss of up to 50% of the initial GSH content. When the culture medium contained 100 microM glutamate and 100 microM cystine, ongoing GSH synthesis counteracted the loss of GSH. The rates of net GSH synthesis were equal for the two groups of aged animals but significantly higher for cells from young controls. It is concluded that externally applied radical scavengers may enhance the protective glutathione 'reserve' of M¿ller cells in cases of neuronal degeneration.

Aging↗
PubMedDate not supplied

Natural extracts as possible protective agents of brain aging.

A growing number of studies suggest that natural extracts and phytochemicals have a positive impact on brain aging. We examined the potential of the Ginkgo biloba extract EGb 761 and red wine-derived constituents on cell death produced by beta-amyloid (Abeta) peptides and oxidative stress, with respect to their possible deleterious role in age-related neurological disorders. We found that EGb 761, possibly through the antioxidant properties of its flavonoids, was able to protect hippocampal cells against toxic effects induced by Abeta peptides. Moreover, we showed that an exposure of rat hippocampal cells to the nitric oxide (NO) donor sodium nitroprusside (SNP) resulted in a decrease in cell survival and increase in reactive oxygen species (ROS) accumulation. However, EGb 761 and red wine-derived polyphenols protected against these events, due to their antioxidant activities, and their ability to block SNP-stimulated activity of protein kinase C (PKC). Taken together, these results support the hypothesis that dietary intake of natural substances may be beneficial in normal aging of the brain.

Aging↗
PubMed2002

EGb 761 is a neuroprotective agent against beta-amyloid toxicity.

Beta-amyloid (Abeta) deposition likely plays a causal role in the lesions that occur in Alzheimer's disease (AD). The Ginkgo biloba extract EGb 761 is widely prescribed in the treatment of cognitive deficits that are associated with normal and pathological brain aging such as AD. We have investigated here the potential effectiveness of EGb 761 against cell death produced by Abeta fragments on primary cultures of hippocampal cells, these cells being severely damaged in AD. A co-treatment with EGb 761 protected cells against toxicity induced by Abeta fragments in a concentration dependent manner. The effect of EGb 761 was even significant if added up to 8 hr to cells and was shared by its flavonoid fraction CP 205, whereas the terpenes bilobalide and ginkgolide B were ineffective. EGb 761 also displayed protective effects against toxicity produced by either H2O2 or nitric oxide, two neurotoxic agents that possibly mediate Abeta toxicity. Moreover, EGb 761, and to a lesser extent CP 205, completely blocked Abeta-induced events, such as reactive oxygen species accumulation and apoptosis. Taken together, these results and those obtained by other groups highlight the neuroprotective abilities of EGb 761 against dysfunction and death of neurons caused by Abeta deposits.

Amyloid beta-Peptides↗