[The antihypoxic and antioxidant action of medicinal plants as the basis for their use in destructive brain diseases].
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Results for “Ginkgo Extract”
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An assessment of the effect of Ginkgo Biloba EGb 761 on ischemia reperfusion injury of intestine.
BACKGROUND/AIMS: The aim of this study was to determine the effect of Ginkgo Biloba (EGb 761) on reperfusion injury of the small bowel. METHODOLOGY: Forty-eight male 200-250 g Spraque-Dawley rats in six groups were used to determine the biochemical and histopathological changes after a 30-min ischemia and 30-min reperfusion. Pre-treatment with 50 mg/kg EGb 761 (Tebofortan, Karlsruhe-Germany) or 10-mL/kg saline was administered intravenously in the treatment and control groups. The superior mesenteric artery was occluded distal to the right colic artery and collateral arcades were ligated to provide complete ischemia. Ischemia was determined by the existence of pulseless or pale color of the small intestine. The return of the pulses and the reestablishment of the pink color were assumed to be the reperfusion of the intestine. Rats that were administered Egb 761 and saline were subjected to laparotomy, ischemia, or ischemia-reperfusion procedures. Mucosal lesions were graded from 0 to 5 in histopathological examination. Malondialdehyde and myeloperoxidase levels of the intestinal mucosa were measured. RESULTS: No significant difference was noted between the control and treatment groups regarding the histopathological changes. Although malonyldialdehyde and myeloperoxidase levels of the reperfusion + EGb 761 group were slightly higher than the laparotomy + saline group, they were significantly lower than the reperfusion + saline group. CONCLUSIONS: We concluded that EGb 761 pre-treatment before ischemia-reperfusion decreased malondialdehyde and myeloperoxidase levels and attenuated the mucosal damage.
Animals↗
Peroxynitrite cytotoxicity on bovine retinal pigmented epithelial cells in culture.
Peroxynitrite induced in vitro a dose dependent toxicity on retinal pigmented epithelial (RPE) cells. Cell death was partially mediated by apoptosis as demonstrated by nuclear fragmentation and TdT-mediated dUTP nick-end labeling assay. Peroxynitrite-induced tyrosine nitration was revealed by immunocytochemistry, both in the cytoplasm and in the nucleus of the cells. Nitration was not observed in RPE cells, producing nitric oxide (NO) after stimulation by lipopolysacharide and interferon-g (IFN-gamma), suggesting that peroxynitrite was not formed in vitro in such conditions. Peroxynitrite could be responsible for the retinal damages observed in pathological conditions in which NO has been demonstrated to be involved. In this context, EGb761, identified as a free radical scavenger, was showed herein to protect RPE cells against peroxynitrite injury.
Animals↗
Evaluation of the dissolution behaviour of some commercial herbal drugs and their preparations.
Dissolution rates are routinely performed with synthetic drugs, however, in the field of herbal drugs (HD), their preparations (HDP) and herbal medicinal products (HMP) this crucial property is generally not investigated. According to the European Pharmacopoeia, we have evaluated the dissolution behaviour of capsules containing various herbal drugs (Passira, Senna, Ginkgo) and some of their commercial dried extracts, manufactured with different methods, by analysis of their active components or marker constituents. Adequate dissolution behaviours of the flavonoids of Ginkgo were obtained for all preparations, while for both Passiflora and Senna only the extracts showed complete dissolution of the marker flavones and sennosides, respectively, in the investigated media.
Biological Availability↗
[Pharmacological correction of cochleovestibular impairments].
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Adult↗
[The hemorheological effects of Lychnis chalcedonica L. extracts].
The hemorrheological effects of extracts from Maltese cross campion (Lychnis chalcedonica L.) prepared using 40% (I) and 70% (II) aqueous ethanol solutions were studied in vitro in comparison with tanakan on the model of high blood viscosity syndrome. Under the hyperthermia conditions, extracts I and II at a concentration of 1 x 10(-5) g/ml limited the growth of blood viscosity and thrombocyte aggregation and the drop in thrombocyte deformability. The effects of both extracts were comparable to those of tanakan. Prolonged (5 days) administration of extract I (daily dose, 150 mg/kg p.o) in rats with arterial hypertension (SHR) decreased the viscosity of whole blood and plasma, reduced the concentration of fibrinogen, and increased the deformability of erythrocytes. No reliable effects of the extracts in vivo upon the erythrocyte aggregation and hematocrit were observed.
Animals↗
Protective effect of ginkgo biloba against gossypol-induced apoptosis in human lymphocytes.
Ginkgo biloba (EGb 761) is a well-defined plant extract that directly scavenges hydroxyl radicals. It is a potent antioxidant that inhibits apoptosis in cultured cells and is effective in treating mild-to-moderate dementia in Alzheimer patients. Apoptosis is an active process of cell destruction and it plays an important role in pathological processes. The aim of this study is to investigate the anti-apoptotic effect of EGb 761 in gossypol-treated human lymphocytes. Pretreatment of lymphocytes with 10 microg/ml EGb 761 for 30 min or 1h decreased the percentage of apoptosis to 17.5% and 20%, respectively. EGb 761 treatment (25-150 microg/ml) decreased the level of apoptosis to a plateau between 8 and 10% of the control values. We conclude that EGb 761 reduces gossypol-induced apoptosis in human lymphocytes.
Apoptosis↗
[Tanakan in the treatment of primary manifestations of insufficiency of brain blood supply].
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[Overview of phytopharmaceuticals for therapy of dementia. Quality and activity of Gingko biloba extract].
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Dementia↗
[Paroxysmal non-hereditary angioedema].
Recurrent hypovolaemic shock had been occurring over the last five and four years, respectively, in a 53-year-old woman and a 46-year-old man who had previously been healthy. The attacks were characterized by a tension feeling and sometimes oedema in the limbs, as well as increased thirst. Within a few hours sweating, tachycardia, orthostatic complaints and shock would occur. The woman's systolic blood pressure would fall to 70 mm Hg and the pulse rate rise to 150/min. The man's blood pressure was not measurable by sphygmomanometer during his first attack. Haematocrit rose to 61 and 71.5%, haemoglobin concentration to 20.7 and 21.3 g/dl, respectively. On administration of plasma expanders all abnormal clinical and biochemical changes quickly disappeared, only to recur within weeks or months. The cause of the condition is an increased permeability of the tissue capillaries, while renal, pulmonary and cerebral vessels apparently are unaffected. During ketotifen and tebonin (gingko biloba extract) administration to the man, he required no further hospitalization for nine months, after which he had three severe attacks. The woman had a severe attack of hypovolaemic shock one month on this treatment. The prognosis of capillary leak syndrome is bad.
Angioedema↗
Ginkgo biloba compared with cholinesterase inhibitors in the treatment of dementia: a review based on meta-analyses by the cochrane collaboration.
Data were derived from the Cochrane Collaboration meta-analyses of the efficacies of ginkgo, donepezil, rivastigmine and galantamine on changes in cognitive function in patients with dementia and, where necessary, were transformed to standardized mean differences. The proportion of patients discontinuing trials was used as a proxy measure of tolerability. Outcomes were assessed after 6 months of treatment. Trial data for cholinesterase inhibitors were more consistent than those for ginkgo, particularly regarding patient populations and outcome measures. Significant benefits on cognition vs. placebo were seen with donepezil, 5 and 10 mg, rivastigmine, 6-12 mg, and galantamine, 16 and 24 mg. Significant benefit vs. placebo with ginkgo was seen only when all doses were pooled. Similar proportions of patients discontinued treatment with ginkgo and placebo. Cholinesterase inhibitors were also well tolerated, although a significantly greater proportion of patients receiving active treatment discontinued vs. placebo with some doses. An evidence-based medicine approach, taking into account the quality of clinical trials, is essential when assessing the safety and efficacy of medications.
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Effects of an extract of Gingko biloba on bromethalin-induced cerebral lipid peroxidation and edema in rats.
The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined. Gingko biloba extract was given (100 mg/kg) by gavage immediately after bromethalin (1.0 mg/kg) administration. Rats were euthanatized at 24 hours after dosing. Brain lipid peroxidation was determined by measurement of brain malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration, brain sodium concentration, and brain water content. Treatment of bromethalin-dosed rats (10/group) with EGB was associated with a statistically significant (P less than 0.05) decrease in clinical sign severity, compared with bromethalin-dosed saline solution-treated rats. All rats given bromethalin and saline solution developed clinical signs of toxicosis including CNS depression, hind limb weakness, ataxia, paralysis, and coma. Some rats given bromethalin and EGB developed clinical signs, however, none developed hind limb paralysis. The brain MDA-TBA concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (80.3 +/- 0.30%), and brain sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were significantly increased in rats given bromethalin and saline solution, compared with control rats given saline solution (1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1 +/- 0.33% water in brain tissue; 4.83 +/- 0.30 mg of brain Na+/g of dry weight) and rats given bromethalin and EGB (1.6 +/- 0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31% water in brain tissue; 5.37 +/- 0.34 mg of brain Na+/g of dry weight).(ABSTRACT TRUNCATED AT 250 WORDS)
Aniline Compounds↗
Natural antioxidants and neurodegenerative diseases.
Neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's (PD) diseases are defined by a progressive neuronal dysfunction and an ensuing behavioral dysfunction. Although protein aggregation (i.e beta-amyloid and alpha-synuclein) plays a pivotal role in both AD and PD, there is increasing evidence that excessive accumulation of reactive oxygen species (ROS) that occurs during normal and pathological brain aging contributes to neuronal losses and dysfunction. Based on these observations, it has been hypothesized that natural antioxidants derived from food, beverages and natural extracts may be beneficial to prevent or delay the occurrence of age-related cognitive deficits and neurodegenerative diseases. We will summarize in this review the role of oxidative stress in pathological brain aging, and provide evidence for a role for antioxidant molecules as therapeutic agents. We will also focus on the various mechanisms underlying their neuroprotective effects in in vivo and in vitro models of neurotoxicity.
Acetylcarnitine↗
The effect of Ginkgo biloba on memory in healthy male volunteers.
The purpose of this study was to investigate possible effects of Ginkgo biloba, a widely used herbal extract, on memory. This study incorporated a double-blind, placebo-controlled design, which used 30 healthy male subjects in each of two groups. The treatment group received two 60-mg tablets of BioGinkgo (27/7) [corrected] daily for 5 days, while the placebo group received a placebo. On the fifth day, after a 2-h waiting period, all subjects were given the Sternberg Memory Scanning Test [Q. J. Exp. Psychol. 27 (1975) 1.], a reaction time control test, the vocabulary and digit span subtests of the WAIS-R [Wechsler D. Manual for the Wechsler adult intelligence scale - revised. New York: Psychological Corporation, 1981.], a reading span test [J. Verbal Learn. Verbal Behav. 19 (1980) 450.] and a prose recall test [Discourse Proc. 13 (1990) 387.]. Blood pressure, heart rate and side effects were also monitored throughout the study. Nonsignificant results were found on all interactions involving treatment group on all tests except the Sternberg Memory Scanning Test. The extract appeared to be safe but largely ineffective in enhancing memory.
Adult↗
Effects of SOD, catalase, and a novel antiarrhythmic drug, EGB 761, on reperfusion-induced arrhythmias in isolated rat hearts.
Effects of superoxide dismutase (SOD), catalase, EGB 761 (Tanakan), and their combination on reperfusion-induced ventricular fibrillation (VF), tachycardia (VT), and the formation of oxygen free radicals were studied after 30 min of global ischemia followed by reperfusion in isolated rat hearts. In the first series of studies, rats received a daily dose of 10(4), 2 x 10(4), or 5 x 10(4) U/kg of SOD (i.v.); 2.5 x 10(4), 5 x 10(4), or 10(5) U/kg of catalase (i.v.); and 25, 50, 100, or 200 mg/kg of EGB 761 (per os), respectively, for 10 d (chronic administration). Neither SOD nor catalase alone reduced the incidence of reperfusion arrhythmias, but EGB 761 dose-dependently reduced the incidence of such arrhythmias. The coadministration of SOD (5 x 10(4) U/kg) with catalase (5 x 10(4) U/kg) significantly reduced the incidence of VF and VT. The same reduction in the incidence of VF and VT was observed when SOD (5 x 10(4) U/kg) was given in combination with EGB 761 (50 mg/kg). In the second series of studies, hearts were isolated and perfused with 5 x 10(4) U/l of SOD plus 5 x 10(4) U/l of catalase (acute treatment), and the incidence of reperfusion-induced VF and VT was significantly reduced. The combination of SOD (5 x 10(4) U/l) with EGB 761 (50 mg/l) also reduced the incidence of VF and VT. In these experiments, we studied the time course of oxygen radical formation using 5,5-dimethyl-pyrroline-N-oxide (DMPO), a spin trap, and it was found that EGB 761 (200 mg/l) or the coadministration of EGB 761 (50 mg/l) with SOD (5 x 10(4) U/l) almost completely abolished the formation of oxygen radicals during reperfusion measured by electron spin resonance (ESR) spectroscopy. Although SOD or catalase alone significantly reduced the formation of oxygen radicals, these drugs failed to prevent the development of reperfusion arrhythmias, while their combination significantly attenuated both the formation of free radicals and the incidence of reperfusion-induced arrhythmias. Our results indicate that the combination therapy may synergistically reduce the formation of free radicals and the incidence of reperfusion-induced VF and VT.
Animals↗
Extract EGb 761 pretreatment limits ubiquitin positive aggregates in rabbit spinal cord neurons after ischemia-reperfusion.
1. Ubiquitin immunohistochemistry was used for investigation of time dependent changes of ubiquitin in the nerve cells reacting to ischemic/reperfusion damage. In the rabbit spinal cord ischemia model a period of 30 min ischemia followed by 24 and 72 h of reperfusion caused neuronal degeneration selectively in the ventral horn motor neurons as well as interneurons of the intermediate zone. 2. Ubiquitin aggregates were accumulated in the neurons of lamina IX and the neurons of intermediate zone destined to die 72 h after 30 min of the spinal cord ischemia. 3. The activation of ubiquitin hydrolytic system is related to a defective homeostasis and could trigger different degenerative processes. Having in mind this, we used EGb 761 to rescue the motor neurons and interneurons against ischemia/reperfusion damage. Our results show that after 30 min of ischemia and 24 or 72 h of reperfusion with EGb 761 pre-treatment for 7 days the vulnerable neurons in the intermediate zone and lamina IX exhibit marked elevation of ubiquitin-positive granules in the cytoplasm, dendrites and nuclei. Abnormal protein aggregates have not been observed in these cells. 4. The rabbits were completely paraplegic after 30 min of ischemia and 24 or 72 h of reperfusion. However, after 7 days EGb 761 pre-treatment, 30 min of ischemia and 24 or 72 h of reperfusion the animals did not show paraplegia. 5. Evaluated ubiquitin-positive neurons of the L(5)-L(6) segments showed significant decrease in number and significant increase of density after 30 min of ischemia followed by 24 h and mainly 72 h of reperfusion. Ubiquitin immunohistochemistry confirmed the protective effect of EGb 761 against ischemia/reperfusion damage in the rabbit spinal cord.
Animals↗
Ginkgolide B inhibits the neurotoxicity of prions or amyloid-beta1-42.
BACKGROUND: Neuronal loss in Alzheimer's or prion diseases is preceded by the accumulation of fibrillar aggregates of toxic proteins (amyloid-beta1-42 or the prion protein). Since some epidemiological studies have demonstrated that the EGb 761 extract, from the leaves of the Ginkgo biloba tree, has a beneficial effect on Alzheimer's disease, the effect of some of the major components of the EGb 761 extract on neuronal responses to amyloid-beta1-42, or to a synthetic miniprion (sPrP106), were investigated. METHODS: Components of the EGb 761 extract were tested in 2 models of neurodegeneration. SH-SY5Y neuroblastoma cells were pre-treated with ginkgolides A or B, quercetin or myricetin, and incubated with amyloid-beta1-42, sPrP106, or other neurotoxins. After 24 hours neuronal survival and the production of prostaglandin E2 that is closely associated with neuronal death was measured. In primary cortical neurons apoptosis (caspase-3) in response to amyloid-beta1-42 or sPrP106 was measured, and in co-cultures the effects of the ginkgolides on the killing of amyloid-beta1-42 or sPrP106 damaged neurons by microglia was tested. RESULTS: Neurons treated with ginkgolides A or B were resistant to amyloid-beta1-42 or sPrP106. Ginkgolide-treated cells were also resistant to platelet activating factor or arachidonic acid, but remained susceptible to hydrogen peroxide or staurosporine. The ginkgolides reduced the production of prostaglandin E2 in response to amyloid-beta1-42 or sPrP106. In primary cortical neurons, the ginkgolides reduced caspase-3 responses to amyloid-beta1-42 or sPrP106, and in co-culture studies the ginkgolides reduced the killing of amyloid-beta1-42 or sPrP106 damaged neurons by microglia. CONCLUSION: Nanomolar concentrations of the ginkgolides protect neurons against the otherwise toxic effects of amyloid-beta1-42 or sPrP106. The ginkgolides also prevented the neurotoxicity of platelet activating factor and reduced the production of prostaglandin E2 in response to platelet activating factor, amyloid-beta1-42 or sPrP106. These results are compatible with prior reports that ginkgolides inhibit platelet-activating factor, and that platelet-activating factor antagonists block the toxicity of amyloid-beta1-42 or sPrP106. The results presented here suggest that platelet-activating factor antagonists such as the ginkgolides may be relevant treatments for prion or Alzheimer's diseases.
Journal Article↗
Lipid peroxidation in experimental spinal cord injury. Comparison of treatment with Ginkgo biloba, TRH and methylprednisolone.
Ischaemia-induced lipid peroxidation is one of the most important factors producing tissue damage in spinal cord injury. In our study, the protective effects of Ginkgo biloba, thyroid releasing hormone (TRH) and methylprednisolone (MP) on compression injury of the rat spinal cord were investigated. For this study 45 rats in four groups, including control, MP, TRH and Gingko biloba, were used to determine the formation of malondialdehyde (MDA). All the animals were made paraplegic by the application clip method of Rivlin and Tator. Rats were divided randomly and blindly to one of four treatment groups (ten animals in each). MP and Ginkgo biloba treatments significantly decreased MDA levels (F = 54.138, P < 0.01). These results suggest that MP and Ginkgo biloba may have a protective effect against ischaemic spinal cord injury by the antioxidant effect.
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