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Clinical Studies
References
A herbal extract from the oldest tree known to man, ginkgo biloba has been double-blind tested many times for its ability to increase the oxygen content to the brain and other bodily tissues. It has been shown to promote mental clarity and concentration, increase alertness and short-term memory and has been used preventatively in regenerative compounds for loss of memory and senility, in cardiac protection formulas against stroke and atherosclerosis and for hearing disorders and vertigo (dizziness) where blood flow is poor in the ears.
It also offers significant protective action against the development of Alzheimer's disease, hearing loss and strokes, and it protects arterial walls. It is known to enhance mental acuity. Some research has shown that Ginkgo Biloba increases cerebral blood flow to the brain. Also, it boosts brain levels of adenosine triphosphate and scavenges free radicals. Combined with ginger, gingko has also been shown too reduce stress induced anxiety.
Ginkgo Biloba may be beneficial in cerebrovascular disease, peripheral vascular insufficiency, arrhythmias, asthma, impotence, premenstrual syndrome, senile macular degeneration, hearing loss, tinnitus, vestibular disorders, age-related cognitive decline, depression, Alzheimer's disease and intermittent claudication.
Published Clinical Studiesclin
The effects of gingko biloba extract (EGb 761) on experimental acute pancreatitis.1
Zeybek N, Gorgulu S, Yagci G, Serdar M, Simsek A, Kaymakcioglu N, Deveci S, Ozcelik H, Tufan T.
Department of Surgery, Gulhane Military Medical Academy, Ankara, Turkey
Acute pancreatitis is an important and fatal disease with high mortality and morbidity. Although the pathogenesis of acute pancreatitis is poorly understood, there are many studies that suggest the role for oxygen free radicals (OFRs) in the development of pancreatitis and its complications and show beneficial effects of scavenger treatment. In the present study, we aimed to investigate whether Egb761, the standardized extract of gingko biloba, restrains the generation of OFRs and ameliorates the histopathologic findings of acute pancreatitis.Sixty male Sprague Dawley rats were randomly assigned to one of the following experimental groups. In early and late pancreatitis and treatment groups, acute pancreatitis was induced by retrograde infusion of 3% sodium taurocholate. In treatment groups, 100 mg/kg Egb 761 was given intraperitoneally (IP) 24 h and immediately before induction of pancreatitis. Sham-operated rats received isotonic saline instead of sodium taurocholate. After observation times of 3.5 and 12 h, the pancreas was removed for light microscopy and determination of malondialdehyde (MDA) levels as a marker for OFRs-induced lipid peroxidation. Serum samples also were obtained for amylase and lipase levels.There was no significant difference in control and sham-operated groups in terms of histopathologic findings and serum enzyme levels. The tissue concentrations of MDA and serum enzyme levels were significantly elevated in early and late treatment groups as compared with the control group. The treatment with Egb 761 caused significant decrease in serum amylase and lipase levels and histopathologic scores as compared with early and late pancreatitis groups.Prophylactic application of Egb761 exerts highly beneficial influence on the course of acute pancreatitis, and this seems to be related to the oxygen radical scavenger effect of Egb761.
PMID: 14697296 [PubMed - in process]
Therapeutic mechanism of ginkgo biloba exocarp polysaccharides on gastric cancer.2
Xu AH, Chen HS, Sun BC, Xiang XR, Chu YF, Zhai F, Jia LC.
Medical College, Yangzhou University, Yangzhou 225001, Jiangsu Province, China. yzxih@21cn.com
AIM: To study the therapeutic mechanism of Ginkgo biloba exocarp polysaccharides (GBEP) on gastric cancer. METHODS: Thirty patients with gastric cancer were treated with oral GBEP capsules. The area of tumors was measured by electron gastroscope before and after treatment, then the inhibitory and effective rates were calculated. The ultrastructures of tumor cells were examined by transmissional electron microscope. Cell culture, MTT, flow cytometry were performed to observe proliferation, apoptosis and changes of relevant gene expression of human gastric cancer SGC-7901 cells. RESULTS: Compared with the statement before treatment, GBEP capsules could reduce the area of tumors, and the effective rate was 73.4%. Ultrastructural changes of the cells indicated that GBEP could induce apoptosis and differentiation in tumor cells of patients with gastric cancer. GBEP could inhibit the growth of human gastric cancer SGC-7901 cells following 24-72 h treatment in vitro at 10-320 mg/L, which was dose- and time-dependent. GBEP was able to elevate the apoptosis rate and expression of c-fos gene, but reduce the expression of c-myc and bcl-2 genes also in a dose-dependent manner. CONCLUSION: The therapeutic mechanism of GBEP on human gastric cancer may relate to its effects on the expression of c-myc, bcl-2 and c-fos genes, which can inhibit proliferation and induce apoptosis and differentiation of tumor cells.
Publication Types:
PMID: 14606069 [PubMed - indexed for MEDLINE]
3
Mechanisms for the vasodilations induced by Ginkgo biloba extract and its main constituent, bilobalide, in rat aorta.
Nishida S, Satoh H.
Department of Pharmacology, Division of Crude and Herbal Medicine, Nara Medical University, Kashihara, Nara 634-8521, Japan.
Vasodilating actions of Ginkgo biloba extract (GBE) and bilobalide, a main constituent, were examined using rat aorta ring strips. GBE at the concentration ranges from 0.03 to 3 mg/ml had a potent concentration-dependent relaxation, reaching 70 +/- 4.5% (n = 6, P < 0.001) at 3 mg/ml. Bilobalide at 0.1 to 100 microM also caused the relaxation in a concentration-dependent manner. At 100 microM, bilobalide caused dilation by 17.6 +/- 3.9% (n = 7, P < 0.05). NG-monomethyl-L-arginine acetate (L-NMMA)(100 microM), an NO synthesis inhibitor, reduced the vasodilation of GBE (3 mg/ml) to 57.6 +/- 2.5% (n = 6, P < 0.05), and was accompanied with a decrease in the rate of relaxation. Tetraethylammonium (TEA)(100 microM), a Ca(2+)-activated K(+) channel inhibitor, also decreased the GBE (3 mg/ml)-induced relaxation to 63.1 +/- 4.6% (n = 6), but not significantly. Indomethacin tended to reduce the GBE (3 mg/ml)-induced vasorelaxation to 67.3 +/- 4.1% (n = 6). In contrast, the vasorelaxation of GBE (3 mg/ml) was strongly attenuated to 53 +/- 6.1% (n = 7, P < 0.05) in Ca(2+)-free medium. Similarly, the vasorelaxation induced by bilobalide significantly decreased both by pretreatment with NO inhibitor (L-NMMA) and in Ca(2+)-free solution. These results indicate that the relaxation induced by GBE would be due to the inhibition of Ca(2+) influx through the Ca(2+) channel and the activation of NO release, and might be in part due to the inhibitions of Ca(2+)-activated K(+) current and PGI(2) release, in the endothelium and aortic vascular muscles. Bilobalide possesses the similar mechanisms for the vasodilation.
PMID: 12672511 [PubMed - indexed for MEDLINE]
The use of Ginkgo biloba in Raynaud's disease: a double-blind placebo-controlled trial.4
Muir AH, Robb R, McLaren M, Daly F, Belch JJ.
Peripheral Vascular Diseases Research Unit, University Department of Medicine, Ninewells Hospital & Medical School, Dundee, UK. a.h.muir@dundee.ac.uk
Raynaud's phenomenon (RP) is a common and painful condition characterized by episodic digital ischaemia produced by emotion and cold. Treatment of RP is notoriously difficult because of the high incidence of side effects. The aim of our study was to investigate the clinical efficacy of a standardized Ginkgo biloba extract (Seredrin) in the treatment of RP in patients with no apparent, associated condition such as systemic sclerosis. A two-week assessment period was done during which patients were asked to record frequency, severity and duration of attacks in diaries. Subjects were then randomized independently of the study centre to receive either active or placebo treatment for 10 weeks, during which time the same data were recorded in their diaries. Patients were seen after two and four weeks of treatment and at the end of the 10-week treatment phase. Blood samples pre- and post-treatment were taken for haemorrheology. Only in the number of attacks per day was there a significant effect of treatment over placebo. The number of attacks per week prior to treatment with Seredrin was 13.2 +/- 16.5 reducing to 5.8 +/- 8.3, a reduction of 56%, whereas placebo reduced the number by only 27% (p < or = 0.00001). There were no significant differences in haamorrheology between the two groups. Ginkgo biloba phytosome may be effective in reducing the number of Raynaud's attacks per week in patients suffering from Raynaud's disease.
Publication Types:
PMID: 12710841 [PubMed - indexed for MEDLINE]
Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo.5
Parsad D, Pandhi R, Juneja A.
Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. dprs@satyam.net.in
For effective treatment of vitiligo, it is as important to arrest the progression of the disease as it is to induce repigmentation. Recently, oxidative stress has been shown to play an important role in the pathogenesis of vitiligo. Ginkgo biloba extract has been shown to have antioxidant and immunomodulatory properties. In a double-blind placebo-controlled trial, we evaluated the efficacy of G. biloba extract in controlling the activity of the disease process in patients with limited and slow-spreading vitiligo and in inducing repigmentation of vitiliginous areas. Fifty-two patients were assigned to two treatment groups (A and B) in a double-blind fashion, but only 47 patients could be evaluated, because one patient in group A and four patients in group B withdrew for reasons unrelated to the study. Patients in group A were given G. biloba extract 40 mg three times daily whereas patients in group B received placebo in similar doses. A statistically significant cessation of active progression of depigmentation was noted in patients treated with G. biloba (P = 0.006). Marked to complete repigmentation was seen in 10 patients in group A, whereas only two patients in group B showed similar repigmentation. The G. biloba extract was well tolerated. G. biloba extract seems to be a simple, safe and fairly effective therapy for arresting the progression of the disease.
Publication Types:
PMID: 12780716 [PubMed - indexed for MEDLINE]
6
Prevention of age-related spatial memory deficits in a transgenic mouse model of Alzheimer's disease by chronic Ginkgo biloba treatment.
Stackman RW, Eckenstein F, Frei B, Kulhanek D, Nowlin J, Quinn JF.
Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR 97239-3098, USA. stackman@ohsu.edu
Alzheimer's disease (AD) is characterized by cognitive decline and deposition of beta-amyloid (Abeta) plaques in cortex and hippocampus. A transgenic mouse AD model (Tg2576) that overexpresses a mutant form of human Abeta precursor protein exhibits age-related cognitive deficits, Abeta plaque deposition, and oxidative damage in the brain. We tested the ability of Ginkgo biloba, a flavonoid-rich antioxidant, to antagonize the age-related behavioral impairment and neuropathology exhibited by Tg2576 mice. At 8 months of age, 16 female Tg2576 and 15 female wild-type (wt) littermate mice were given ad lib access to tap water or Ginkgo biloba (70 mg/kg/day in water). After 6 months of treatment, all mice received Morris water maze training (4 trials/day for 10 days) to assess hippocampal dependent spatial learning. All mice received a 60-s probe test of spatial memory retention 24 h after the 40th trial. Untreated Tg2576 mice exhibited a spatial learning impairment, relative to wt mice, while Ginkgo biloba-treated Tg2576 mice exhibited spatial memory retention comparable to wt during the probe test. Spatial learning was not different between Ginkgo biloba-treated and untreated wt mice. There were no group differences in learning to swim to a visible platform. Soluble Abeta and hippocampal Abeta plaque burden did not differ between the Tg2576 groups. Brain levels of protein carbonyls were paradoxically elevated in Ginkgo biloba-treated mice. These data indicate that chronic Ginkgo biloba treatment can block an age-dependent decline in spatial cognition without altering Abeta levels and without suppressing protein oxidation in a transgenic mouse model of AD.
PMID: 14637120 [PubMed - indexed for MEDLINE]
Neuroprotective effects of Ginkgo biloba extract.7
Ahlemeyer B, Krieglstein J.
Institut fur Pharmakologie und Toxikologie, Fachbereich Pharmazie der Philipps-Universitat Marburg, Ketzerbach 63, 35032 Marburg, Germany.
Ginkgo biloba extract has been therapeutically used for several decades to increase peripheral and cerebral blood flow as well as for the treatment of dementia. The extract contains multiple compounds such as flavonoids and terpenoids that are thought to contribute to its neuroprotective and vasotropic effects. In this review, we summarize the experimental results on the mechanism of neuroprotection induced by standardized extract of Ginkgo biloba leaves (EGb 761) and its constituents. The effects described mostly in animals include those on cerebral blood flow, neurotransmitter systems, cellular redox state and nitric oxide level. Furthermore, we discuss the current status of clinical trials as well as undesired side effects of EGb 761.
Publication Types:
PMID: 14523543 [PubMed - indexed for MEDLINE]
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8
Ginkgo biloba normalises stress-elevated alterations in brain catecholamines, serotonin and plasma corticosterone levels.
Shah ZA, Sharma P, Vohora SB.
Department of Medical Elementology and Toxicology, Faculty of Science, Hamdard University, 110 062 New Delhi, India.
Stress and depression and associated mental health problems have increased tremendously in modern times. The search for effective and safe alternatives from natural sources especially plant products should, therefore, continue. Forced immobilization is one of the best explored models of stress in rats and the role of corticosterone, serotonin and catecholamines, i.e. norepinephrine (NE), dopamine (DA) is well documented. Numerous studies have shown that Ginkgo biloba has antioxidant and neuroprotective properties and utility in cerebrovascular insufficiency and impaired cerebral performance. We investigated the effect of G. biloba on whole brain catecholamine, serotonin and plasma corticosterone levels following 1, 2 and 4 h restraint stress using HPLC and also plasma corticosterone using luminescence spectrophotometry. G. biloba extract (14 mg/kg p.o.) restored restraint stress-induced elevation in whole brain levels of catecholamines (NE, DA), 5-HT and plasma corticosterone to near normal levels. Further studies are warranted to explore the clinical potential of this encouraging lead in the management of stress and to elucidate the mechanisms involved.
PMID: 12957329 [PubMed - indexed for MEDLINE]
Evaluation of nitric oxide scavenging activity of certain spices in vitro: a preliminary study.9
Baliga MS, Jagetia GC, Rao SK, Babu K.
Department of Radiobiology Kasturba Medical College, Manipal-576 119, Karnataka, India.
The plant extracts of some commonly used spices were examined for their possible regulatory effect on nitric oxide (NO) levels using sodium nitroprusside as a NO donor in vitro. Most of the extracts tested demonstrated direct scavenging of NO and exhibited significant activity and the potency of scavenging activity was in the following order: Foeniculum vulgare (aqueous) > Citrus limettiodes > Murraya koenigii (seed, aqueous) > Murraya koenigii (leaf, aqueous) > Curcuma aromatica (aqueous) > Murraya koenigii (leaf, dichloromethane:methanol) > Mentha arvensis (chloroform) > Mentha arvensis (aqueous) > Curcuma longa > Gingko biloba > Foeniculum vulgare (dichloromethane:methanol) > Zingiber officinale (aqueous) > Curcuma aromatica (ethanolic) > Murraya koenigii (seed, dichloromethane:methanol). All the evaluated extracts exhibited a dose-dependent NO scavenging activity. The aqueous extract of Foeniculum vulgare showed a greatest NO scavenging effect of 79.75% at 62.5 microg/mL as compared to the positive control, Gingko biloba where 36.22% scavenging was observed at similar concentration. The present results suggest that these spices might be potent and novel therapeutic agents for scavenging of NO and the regulation of pathological conditions caused by excessive generation of NO and its oxidation product, peroxynitrite.
Publication Types:
PMID: 13678266 [PubMed - indexed for MEDLINE]
[Protective effect of ginkgo biloba extract on cerebral ischemia/reperfusion injury in rats]10
Hu B, Sun SG, Mei YW.
Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022. hubo@hust.edu.cn
OBJECTIVE: To study the effect of Ginkgo biloba extract (GbE) on dynamic equilibrium of free radicals and amino-acids in cortex of rats with cerebral ischemia/reperfusion (I/R) injury and its influence and characteristics to intracellular free calcium concentration ([Ca2+]i) in primary cultured hippocampal neuron of rats. METHODS: Amino-acids were quantified by high performance liquid chromatographic (HPLC) analysis. Concentration of MDA and GSH-Px were determined by thiobarbituric acid (TBA) technique. SOD was assayed through xanthine method, and microfluoremetric technique was used to assay the change of [Ca2+]i and its characteristics. RESULTS: Compared with the non-treated groups, at all time points (3 hrs after ischemia, 1 and 2 hrs after I/R separately), in the GbE treated groups, the levels of Glu, Asp and MDA were lower and SOD and GSH-Px were higher (P < 0.01 or P < 0.05), the GABA and Gly levels were lower in groups treated with middle (10 mg/kg) or high dosage (15 mg/kg) of GbE (P < 0.05). Compared with the group treated with small dosage GbE (5 mg/kg), Glu, Asp and MDA were lower and GABA, Gly, SOD and GSH-Px were higher in the groups treated with middle or high dosage of GbE (P < 0.05), while the difference in the latter two groups was insignificant. Level of [Ca2+]i in cultured neurons treated with 1 x 10(-5) mol/L glutamate combined 25 micrograms/ml GbE for 20s was lower with lower peak value and longer time for reaching the peak than that in neurons treated with 1 x 10(-5) mol/L glutamate alone. Besides, the time of decline phase was also shorter in the former, so the flatform stage was prolonged. The response was recovered by re-applying of glutamate after [Ca2+]i back to base line. CONCLUSION: GbE can protect damaged neurons through keeping the balance of inhibitory/excitatory amino-acids, enhancing free radicals scavengers system, and inhibiting the effect of glutamate to [Ca2+]i.
PMID: 12872397 [PubMed - indexed for MEDLINE]
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