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PubMed2003

[Effect of methanol eluates from Ginkgo biloba root on growth and development of arbuscular mycorrhizal fungi cultured in vitro].

The effect of methanol eluates from Ginkgo biloba root on growth and development of arbuscular mycorrhizal fungi was studied under cultured in vitro. The study indicated that the methanol eluates from Ginkgo biloba root could significantly stimulate the spore germination and hyphal growth of arbuscular mycorrhizal fungi (Glomus mosseae, Gigaspora margarita), and the 80% methanol eluates had the most significant effect. There were rich flavonoids in the methanol eluates, and the highest flavonoids content was in the 80% methanol eluates. The mathematical analysis showed that there was a significantly positive correlation between the flavonoids content in the methanol eluates and the growth and development of arbuscular mycorrhizal fungi cultured in vitro.

Dose-Response Relationship, Drug↗
PubMed2005

Antioxidants prevented oxidative injury of SR induced by Fe2+/H2O2/ascorbate system but failed to prevent Ca2+-ATPase activity decrease.

Dysfunction of sarcoplasmic reticulum (SR) Ca2+-ATPase induced by oxidative stress may be a contributing factor to the development of serious age related diseases. Incubation of sarcoplasmic reticulum (SR) vesicles of rabbit skeletal muscles with Fe2+/H2O2/ascorbate decreased the SH group content of SR approximately to 35% and Ca2+-ATPase activity to 50% of control not oxidized sample. Protein carbonyls increased twofold, lipid peroxidation was also significantly elevated. The antioxidant effects of trolox, the pyridoindole derivative stobadine and of the standardized extracts from bark of Pinus Pinaster PycnogenolR (Pyc) and from leaves of Ginkgo biloba (EGb 761) were studied on oxidatively injured SR. All antioxidants exerted preventive effects against the oxidized lipids and protein SH groups of SR vesicles. Trolox and stobadine did not influence protein carbonyl formation, while flavonoid extracts prevented carbonyl generation, probably by binding to protein. The preventive effects of the antioxidants studied on lipids and protein SH groups were however not associated with protection of Ca2+-ATPase activity. Stobadine and trolox exerted no effect on enzyme activity, Pyc and EGb 761 enhanced the inhibitory effect of Ca2+-ATPase activity in oxidatively injured SR. Concluding, under the conditions of oxidative stress induced by Fe2+/H2O2/ascorbate against SR of rabbit skeletal muscle, the agents studied demonstrated antioxidant effects yet failed to protect Ca2+-ATPase activity.

Animals↗
PubMed2004

Drug treatment of intermittent claudication.

The US FDA has approved two drugs for the management of intermittent claudication: pentoxifylline and cilostazol. The mechanism of action that provides symptom relief with pentoxifylline is poorly understood but is thought to involve red blood cell deformability as well as a reduction in fibrinogen concentration, platelet adhesiveness and whole blood viscosity. The recommended dose of pentoxifylline is 400 mg three times daily with meals. Cilostazol is a potent, reversible, phosphodiesterase III inhibitor. The inhibition of phosphodiesterase allows for the increased availability of cyclic adenosine monophosphate (cAMP). cAMP mediates many agonist-induced platelet inhibitory, vasodilatory and vascular antiproliferative responses. Cilostazol, at a dose of 100 mg twice daily, is recommended to be taken 30 minutes before or 2 hours after breakfast and dinner. In addition to pentoxifylline and cilostazol, clinical trials indicate many other drugs may relieve the symptoms of intermittent claudication. Ginkgo biloba, available as an over-the-counter extract, provides symptom relief comparable to pentoxifylline. Two European agents, naftidrofuryl and buflomedil, also have efficacy that is reported to be similar to pentoxifylline. Policosanol is a mixture of fatty alcohols derived from honeybee wax which, according to very limited data, reduces symptoms of claudication. Amino acids, certain peptides and prostaglandins may have a therapeutic role. Finally, novel approaches including angiogenesis mediated by growth factors, are currently under investigation.

Animals↗
PubMed2006

[Ability of catechin to eliminate O2-* and *OH].

OBJECTIVE: To investigate the eliminating ability of catechin to eliminate O2-* and *OH. METHODS: The ability of catechin to clear away O2-* and *OH was respectively measured by faintness chemiluminescence and spin trapping assay. RESULTS: IC50 that catechin eliminated O2-* and *OH was 6.16, 0.59 g/mL respectively, and the eliminating ability of catechin was much stronger than that of the extract from liquorice, rosemary, grape pip, giant knotweed and ginkgo leaf. CONCLUSION: Compared with several important natural plants of antioxidants, the eliminating ability of cathechin is the best.

Antioxidants↗
PubMed2003

Retrobulbar haemorrhage associated with chronic Gingko biloba ingestion.

Retrobulbar haemorrhage is a rare and potentially sight threatening complication after peribulbar local anaesthetic injection for cataract surgery. A case is reported of a woman who developed this complication and was subsequently found to have been taking Gingko biloba extract tablets which may have predisposed her to developing the haemorrhage.

Aged↗
PubMed1992

Ginkgo biloba.

Explore the source record for details and available documents.

Europe↗
PubMed2004

Effects of Ginkgo biloba on alertness and chemosensory function in healthy adults.

Ginkgo biloba is reported to enhance cognitive function in patients with selected neural disorders. Its effects in healthy, young adults are less well characterized. This work explored whether Ginkgo biloba could ameliorate decrements in alertness post-prandially and/or enhance chemosensory function. Both are functions that could be influenced by enhanced cerebral blood flow and neuronal metabolism, reported properties of the compound. A double-blind placebo-controlled study was conducted with 19 males and 20 females with a mean age of 23.6 +/- 5.4 years and mean weight of 70.0 +/- 1.9 kg. Participants were supplemented for 13 weeks with either Ginkgo biloba (mean dose 184.5 mg/d (range 130-234 mg/d)) or placebo and administered various alertness, performance, affective state and chemosensory tests at weeks 1, 5, 9 and 13. Participants did experience the post-prandial affective state decrement (i.e. post-lunch dip), but not the performance decrement. Performance on the chemosensory tests improved over the 13-week study. However, Ginkgo biloba was ineffective at alleviating the symptoms of the post-lunch dip or at enhancing taste and smell function.

Adolescent↗
PubMed2006

Evaluation of antioxidant activity of Ginkgo biloba phytosomes in rat brain.

Ginkgo biloba from the traditional Chinese system of medicine has been found to possess neurocognitive enhancing effects. The mechanism of action of Ginkgo seems to be related to its antioxidant properties. In the present study, Ginkgo biloba phytosomes were administered to Wistar rats at 50 mg/kg and 100 mg/kg for 7 and 14 days. Chemical hypoxia was induced by administration of sodium nitrite (75 mg/kg) 1 h after the last administration of treatment. Thirty minutes after sodium nitrite administration, the animals were killed and the cerebral cortex, cerebellum, hippocampus and striatum were isolated and homogenized. The supernatants were used for the estimation of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. Ginkgo biloba phytosome treatment was found to increase superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities in all the brain regions compared with those treated only with sodium nitrite. The prevention of depletion of the antioxidant enzymes by sodium nitrite in the presence of Ginkgo biloba phytosomes may be correlated to its antioxidant activity.

Animals↗
PubMed2004

Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain.

BACKGROUND: The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats. METHODS: Rats (EMR+) were exposed to 900 MHz EMR from MP for 7 days (1 h/day). In the EMR+Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups. RESULTS: Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically. CONCLUSION: Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue.

Animals↗
PubMed2000

High-performance liquid chromatography-electrospray ionization-mass spectrometry study of ginkgolic acid in the leaves and fruits of the ginkgo tree (Ginkgo biloba).

A method is developed for qualitative analysis of ginkgolic acids in the leaves and fruits of Ginkgo biloba by high-performance liquid chromatography (HPLC)-electrospray ionization-mass spectrometry technique. Negative ionization mode is successful in obtaining a very abundant deprotonated molecule [M - H]-. The mass detection sensitivity is higher than ultraviolet detection but relies heavily on the concentration of acetic acid in the HPLC eluent, which consists of acetonitrile-water-acetic acid. The method is also very specific for the analysis of ginkgolic acid with no interferences from the sample matrix.

Acetic Acid↗
PubMed2006

Current pharmacotherapy for Alzheimer's disease.

Alzheimer's disease (AD) is an age-related neurodegenerative disease that affects approximately 4.5 million people in the United States. The mainstays of current pharmacotherapy for AD are compounds aimed at increasing the levels of acetylcholine in the brain, thereby facilitating cholinergic neurotransmission through inhibition of the cholinesterases. These drugs, known as acetylcholinesterase inhibitors (AChEIs), were first approved by the U.S. Food and Drug Administration (FDA) in 1995 based on clinical trials showing modest symptomatic benefit on cognitive, behavioral, and global measures. In 2004 the FDA approved memantine, an NMDA antagonist, for treating dementia symptoms in moderate to severe AD cases. In clinical practice, memantine may be co-administered with an AChEI, although neither drug individually or in combination affects the underlying pathophysiology of dementia. Dementia in AD results from progressive synaptic loss and neuronal death. As knowledge of the mechanisms responsible for neurodegeneration in AD increases, it is anticipated that neuroprotective drugs to slow or prevent neuronal dysfunction and death will be developed to complement current symptomatic treatments.

Alzheimer Disease↗
PubMed1999

The clinical applications of Ginkgo biloba, St. John's wort, saw palmetto, and soy.

The use of herbal or alternative therapies continues to increase each year. This article extensively reviews four of the more commonly used herbs and dietary supplements: ginkgo biloba, St. John's wort, saw palmetto, and soy. The pharmacology, precautions, therapeutic uses, and adverse effects for each of these therapies are discussed.

Ericales↗
PubMed2001

Natural therapies for ocular disorders, part two: cataracts and glaucoma.

Pathophysiological mechanisms of cataract formation include deficient glutathione levels contributing to a faulty antioxidant defense system within the lens of the eye. Nutrients to increase glutathione levels and activity include lipoic acid, vitamins E and C, and selenium. Cataract patients also tend to be deficient in vitamin A and the carotenes, lutein and zeaxanthin. The B vitamin riboflavin appears to play an essential role as a precursor to flavin adenine dinucleotide (FAD), a co-factor for glutathione reductase activity. Other nutrients and botanicals, which may benefit cataract patients or help prevent cataracts, include pantethine, folic acid, melatonin, and bilberry. Diabetic cataracts are caused by an elevation of polyols within the lens of the eye catalyzed by the enzyme aldose reductase. Flavonoids, particularly quercetin and its derivatives, are potent inhibitors of aldose reductase. Glaucoma is characterized by increased intraocular pressure (IOP) in some but not all cases. Some patients with glaucoma have normal IOP but poor circulation, resulting in damage to the optic nerve. Faulty glycosaminoglycan (GAG) synthesis or breakdown in the trabecular meshwork associated with aqueous outflow has also been implicated. Similar to patients with cataracts, those with glaucoma typically have compromised antioxidant defense systems as well. Nutrients that can impact GAGs such as vitamin C and glucosamine sulfate may hold promise for glaucoma treatment. Vitamin C in high doses has been found to lower IOP via its osmotic effect. Other nutrients holding some potential benefit for glaucoma include lipoic acid, vitamin B12, magnesium, and melatonin. Botanicals may offer some therapeutic potential. Ginkgo biloba increases circulation to the optic nerve; forskolin (an extract from Coleus forskohlii) has been used successfully as a topical agent to lower IOP; and intramuscular injections of Salvia miltiorrhiza have shown benefit in improving visual acuity and peripheral vision in people with glaucoma.

Cataract↗