银杏叶提取物加蝇蛆喂鸡对鸡的免疫性能的影响说明书带开题
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401Ginkgo biloba neuroprotection: Therapeuticimplications in Alzheimers diseaseYuan LuoDepartment of Biological Sciences, Box 5018,University of Southern Mississippi, Hattiesburg, MS39406, USATel.: +1 601 266 5417; Fax: +1 601 266 5797;E-mail: Yuan.LuoAnextractofGinkgobilobaleaves,EGb761, isbecomingoneof the most popular dietary supplements in the United Statesto enhance memory. In Europe it is a commonly prescribeddrug for treatment of age-related deterioration, including de-generativedementiasoftheAlzheimertype(AD).Substantialexperimental evidence indicates that EGb761 has neuropro-tective potency under conditions such as ischemia, seizuresand peripheral nerve damage. However, the mechanisms ofsuch neuroprotective effects remain unknown, partially be-cause of the complex chemical composition of EGb761 andthe resulting so-called “polyvalent” action. This review fo-cuses on cellular and molecular approaches towards under-standing the polyvalent action of EGb761 neuroprotective ef-fect. Two potential mechanisms of action, reducing oxida-tive damage and stimulating cell survival machinery, are dis-cussed. Better understanding of the neuroprotective mecha-nisms of EGb761 will provide impetus for possible combi-nation therapies and for the design of rational, “mechanism-based” strategies that target age-related neurodegenerationand Alzheimers disease.1. IntroductionGinkgo biloba tree, known as “a living fossil”, has alife span of 4000 years, possibly due to its high toler-ance to pollution and resistance to infections 17. Ex-tracts from the Ginkgo biloba leaves have been foundin ancient and modern Chinese herbal pharmacopoeiaas treatment for dysfunctions of heart and lung and aspromoter of longevity 18.Standardized extract ofGinkgo biloba leaves is presently used in Europe asone of the most commonly prescribed drugs for treat-ment of age-related deterioration of mental functions,as well as for treatment of vascular dementia and de-generative dementias of the Alzheimer type (AD) 39,41. In the United States, it is one of the most popularmarketedherbalmedicines, notyetunderthestrict reg-ulation of the Food and Drug Administration (FDA),for enhancement of blood circulation and memory.The standardized extract of Ginkgo biloba leavesnamedEGb761containsspecificpercentagesofginkgo-flavoneglycosides(24%)andterpenoids(6%),thelatergroup consisting of bilobalide and the ginkgolides A,B, C, M, and J 28.It is not certain which sub-stances in EGb761 are responsible for the presumedhealth-enhancing properties.It has been suggestedthat the glycosidespossess antioxidantactivity, andtheginkgolide B, also known as BN52021, is a potent an-tagonist of the platelet-activating factor (PAF) recep-tor 60. Accumulating evidence has suggested thatmany of the actions of EGb761 are so-called “poly-valent” actions, i.e., the clinical responses of EGb761are the net effect of interactions between the vari-ous biological activities of the individualsubstances ofEGb76116. Thisis inagreementwiththephilosophyof Chinese herbal medicine, in which wholesome ef-fectsofamixtureofcompounds,actingsimultaneouslyin combination and synergy, are required to balancebodys yin and yang.2. Neuroprotective effects of EGb761During the past decade, in vivo and in vitro experi-mentsinmammaliansystemsandclinicalstudiesinhu-mandemonstratedthatEGb761exhibitsarangeofbio-chemical and pharmacological effects, which include:vasoregulation,cognitionenhancement,andalleviatingstress 17,62. In human studies, available data haveconfirmed the clinical efficacy of EGb761 in primarydegenerativedementia of Alzheimers type 33,34,41.Although the evidence supporting EGb761 enhance-ment of learning and longevity in healthy animals andhumansisinconclusive16,68,therearesufficientdatato support the view that the extract has neuroprotectiveproperties 60.Journal of Alzheimers Disease 3 (2001) 401407ISSN 1387-2877 / $8.002001, IOS Press. All rights reserved402Y. Luo / Herbal medicine, neuroprotectants, Alzheimers diseaseEGb761 has been shown to protect animals fromeffects of hypoxia 27, ischemia 47, and to reducethe behavioral deficits resulting from brain injury 2.Several lines of evidence indicate that EGb761 coun-ters the effects of stress and aging 53, at least in part,through an increase in the density of -2 adrenore-ceptors 25 and serotonergic (5-HT1A) receptors 24in brain tissue. In isolated synaptosomes from micecerebral cortex, EGb761 treatment elevated 5-HT up-take52,whichisdownregulatedindegeneratedbrain.Choline uptake was also increased in EGb761-treatedhippocampal synaptosomes 31.Choline is a pre-cursor for biosynthesis of the neurotransmitter acetyl-choline, which plays a crucial role in memory andlearning processes. Loss of basal forebraincholinergicneurons has been directly related to AD 3.Synergistically, EGb761 may protect brain by af-fecting cerebral blood flow and energy metabolismin experimental animals.EGb761 treatment re-sulted in an increased blood flow, elevated levels ofATP and glucose in rats 28,34, and reduced lev-els of free fatty acids in hippocampus of rats underseizure conditions 54. Animal behavioral studies byCohen-Salmon et al., suggest that long-term treatmentwith EGb761 reduces some stress-induced behavioralchangesinoldmice43. Theauthorshaveobservedaneffect of EGb761 on improvedperformanceof a learn-ingtask in agedmice chronicallytreatedwith EGb761.Furthermore, they found a statistically significant hip-pocampal structure changes in post mortem histolog-ical analysis of these mice, particularly in the mossyfibers in CA3 region of the hippocampus14. At a re-cent Meeting of Society for Neuroscience, two groupsofinvestigators,workingondifferentsystems,reportedon a possible role of EGb761in neuroregeneration12,19.Ginkgolide B (BN52021), a component of EGb761,may protect neurons by being an antagonist of a recep-tor for the platelet-activating factor (PAF) 60. PAF isan alkylphospholipid produced by a variety of cells; itis one of the most potent lipid mediators known 61.PAF inducesneuronalapoptosis, glutamaterelease andtranscriptional activation following excitotoxic chal-lenge5. PAFconcentrationisknowntoincreaseinthebrain during trauma 27, which results in an increasein free intracellular Ca2+concentration 30. SpecificPAF receptors have been identified in the neurons, lo-calized to intracellular membranes, synaptic endingsandmicroglia 37. Bazanandcolleagueshavedemon-strated that ginkgolide B (BN52021) has impressiveneuroprotective properties 5. Nevertheless, based onthe in vivo animal experiments mentioned above, it isunclear to what extent EGb761 exerts its function di-rectly on central nervous system (CNS).In vitro experimentsindicate that EGb761has directeffectsonCNS. EGb761attenuatedneuronalcelldeathinducedby serumdeprivationandstaurosporinein cul-tured chick embryonic neurons and neonatal rat hip-pocampus1andbyamyloidinprimaryculturedhip-pocampalneurons4. It protectedneuronsagainst ox-idativestress inducedby hydrogenperoxidein dissoci-atedratcerebellarneurons40,42,againstcytotoxicityinducedbycalciumchannelblockersinratcorticalneu-rons72andby glutamatein HT-4 neuronalcells 29.In accord with its role as an anti-oxidant, EGb761 sup-pressed the reactive oxygen species (ROS) formationin anischemia modelof cerebellarneurons42. Largebody of analysis has revealed that, in a cellular or invitro system EGb761 interacts either directly or indi-rectlywith nearlyall ROS of biologicalsignificance. Itnot only meets all of the criteria that are required forcharacterizing a substance as an anti-oxidant 17, butalso could be the most efficacious antioxidant.MitochondriabothgenerateanddetoxifyROS.Thus,imbalance of this compromise plays a key role inchronicdiseases 46. EGb761may preventmitochon-drial aging by its free-radical scavenger effect. In cul-tured cells, EGb761 stimulates mitochondrial gene ex-pression of the respiratory-chain enzyme complex I,which is decreased in several neurodegenerative dis-ease 10.The same author recently suggested thatEGb761 inhibits excitotoxic neuronal death by antag-onizing the effect of glycine 11. Janssens and col-leagues,usingisolatedmitochondriafromrats, demon-strated that EGb761 protects mitochondria againstischemia-induced oxidative stress 26. MitochondrialDNA (mtDNA) is especially susceptible to oxidativedamage and mutations, which, in turn, contributes tomany degenerative diseases 65.Sastre et al.re-cently showed that oral administration of EGb761 torats for 3 month was able to prevent the age-associatedoxidative damage to mtDNA, oxidation of mitochon-drial glutathione, as well as changes in mitochondrialmorphology and function in brain and liver 55,56.These results suggest that EGb761 prevents mitochon-drial aging by attenuating the chronic oxidative stressassociated with this process.3. Possible mechanisms of neuroprotectionConsiderabletheory and some evidencesuggest thatoxidativeimbalance(stress),mitochondrialbioenerget-Y. Luo / Herbal medicine, neuroprotectants, Alzheimers disease403icsdefects,excitatoryneurotoxicity,calciumcytotoxic-ityandtrophicfactordeficienciesmaycontributetocelldeath in neurodegenerative diseases 36,38,44. Cur-rent consensus is that two broad mechanisms, oxida-tive stress and excessive activation of glutamate recep-tors, are converging and represent sequential as wellas simultaneousprocesses that providea final commonpathway for cell vulnerability in the brain 15. Beinga mixture, EGb761 may exert its neuroprotectionin aninteractive, synergistic way, e.g., by inducing the pro-tectivepathwayagainstoxidativestress,andatthesametime inhibiting the apoptotic machinery. The specificpathways are depicted in Fig. 1.Several laboratories demonstrating EGb761 neuro-protection against oxidative stress, excitotoxicity, andneurotoxicity have emphasized possible anti-oxidantproperties of EGb761 as one of its mechanisms of ac-tion 49. EGb761 may act not only as a radical scav-enger: processes downstream of the anti-oxidative ef-fect of EGb761 may also be involved in the inhibitionof apoptosis. For example, EGb761 inhibits lipid per-oxidationandincreasesthelevelsofsuperoxidedismu-tase (SOD), an endogenous antioxidant enzyme sys-tem 63. Even the anti-apoptotic action of EGb761may be mediated by its antioxidative capacity. Also,as a PAF antagonist 7, EGb761 suppresses the PAF-induced generation of reactive oxygen species 6.Among numerous theories raised to explain neu-rodegenerativeAlzheimersdiseases,the“amyloidbeta(A)-inducedfree radical-mediatedneurotoxicity”hy-pothesis 69 is especially attractive because it pro-vides a rationale for intervention. That is, adminis-tration of “exogenous antioxidant” such as EGb761may slow the progress of the disease. According tothis theory, free radicals may be the link between A-induced cellular damage and cytotoxicity in AD. Thishypothesis is based on two observations: 1) aggrega-tion of A, the main constituent in AD plaques, istoxic to neurons 70, thus may initiate and promoteneurodegeneration, and 2) aggregated A protein it-selfspontaneouslygeneratesmorereactiveoxygenrad-icals that can damage the cells 21,22.Additionalexperimental evidence supporting this hypothesis in-cludes: the antioxidant vitamin E protected corticalsynaptosomal membranes and cultured hippocampalneuronsfromA-inducedtoxicity8andEGb761pro-tectedhippocampalneuronsagainstamyloid-inducedcell death 4.However, experimental results fromother laboratories argue against this theory. The Aaggregation-inducedfree radical release 22 has beendescribed as an experimental artifact 20. Mason andcoworker suggested that amyloid peptide (2535)in fact has an antioxidative activity: it inhibited lipidperoxidation in a liposome membrane 66.If freeradicals mediated the A-induced toxicity, an antioxi-dant would block the effect. However, Pike et al. ob-served that antioxidants did not protect against A-induced neurotoxicity in primary cultured rat embry-onic cells 48. Yao and coworkers also demonstratedthat ginkgolides prevented the A-induced increase ofreactive oxygen species (ROS), but that did not rescuethe cells from A-induced apoptosis in cultured PC12cells 71. They concluded that the free radicals andlipidperoxidationdonotmediateA-inducedneuronalcell death.The current understanding is that in vivo oxidativestatus is a dynamic balance between pro-oxidant andoxidant defenses and is yet difficult to determine 58.Even the pathologicallesion of AD, senile plaques andneurofibrillarytangles,mayplayanimportantaspectindefense,i.e. protectionofneuronsfromoxidation46.The discrepancy among those results obtained from invitro studies could be due to differentmodels of oxida-tivestress, differentchemicalsused,differenttreatmentparadigms and the use of different markers for oxida-tion. Giventhatmultiplemarkerswerefoundin vivotobe related to neuronal death in AD 57,59, Perry et alemphasized the importance of appreciating the full ex-tent of protectionfromoxidants46. It is possible thatEGb761,amixtureofmanycompounds,butnotthean-tioxidants ginkgolides and Vitamin E alone, could pre-vent the A-induced toxicity by its polyvalent actionincluding potential effects on A conformation. Evena direct physical interference with the process of Aaggregationcannotbepresentlyexcludedas a potentialmechanism of action of EGb761. Further, the experi-ments mentionedabovewere conductedin vitro, on ei-therartificial membraneor culturedcells. Unequivocalevidence could, perhaps, be obtained by studies usinga transgenic animal model of AD 51.Several laboratories have reported anti-apoptosis ef-fectsofEGb7611,40,42,72,butthemechanismisstillunknown. Recentadvancesinourunderstandingoftheprocesses that control apoptosis include the followingdiscoveries67: 1)Fasreceptormediatesinitialeventsleadingto apoptosis, 2) the release of proteins, particu-larly cytochrome c from mitochondria, triggers activa-tion of caspases, a family of proteolytic enzymes, and3) activation of caspase 3 is critical for the initiationand execution of apoptosis. None of the componentsof the apoptosis pathways have yet been demonstratedto contribute to EGb761 neuroprotective action. How-404Y. Luo / Herbal medicine, neuroprotectants, Alzheimers diseaseNGFRNMDARPAFRGRasPI3 kinaseArkMEKMAPK (JNK)Bcl2cAMPPKAPLCDAGCa+PKCCyt cCaspase 9Caspase 3DNA fragmentationApoptosisSurvivalAC12-MAPKKKOXPHOSMit. damageO2- .BAX34Fig. 1. Potential mechanisms whereby EGb761 may exert neuroprotective effects. 1) EGb761 may stimulate NGFR (nerve growth factorreceptor)/PI3 kinase-mediated cell survival pathway for its protective effect against apoptosis induced by serum deprivation. 2) EGb761 mayinhibit PAFR (platelet activating actor receptor)- and/or NMDAR (NMDA receptor)-mediated apoptosis pathway, involving G (G protein subunit), PKC (protein kinase C) and MAPK cascade (MAPKKK MEK MAP kinase). 3) As an antioxidant, EGb761 may function as afree radical scavenger, and an inhibitor of free radical production. Thus, protect cells from oxidative damage. 4) EGb761 may prevent cellularaging by targeting at mitochondria cell death machinery. Both the pro-apoptotic factor Bax and the anti-apoptotic factor Bcl2 are located onmitochondria (Mit). Under multiple stimuli, BAX activates caspases-3 by releasing cytochrome c (Cyt c) from mitochondria. Caspase 3 thenact on intracellular substrates to execute the cell death program. Other pathways include PKA (protein kinase A)-mediated survival pathway andRas/MAPK cascade-mediated cell proliferation/differentiation pathway; AC: adenyly cyclase; OXPHOS, oxidative phosphorylation; (Ca2+)i:intracellular calcium concentration. The dashed lines indicate alternative pathways. A circle with “” represents an inhibitory pathway.ever, as a PAF antagonist, EGb761 may mediate neu-roprotection, at least partially, by a signal transductionpathway similar to those used by nerve growth factor(NGF). PAF is a potent phospholipid mediator, whichelicits a diverse array of biological actions by interact-ing with G protein-coupled PAF receptor (PAFR) 9.PAFR expression is associated with neuronal apopto-sis 5. PAF enhances excitatory synaptic transmissionin the hippocampus by activating pre-synaptic PAF re-ceptors 13. In most PAF-responsive cells, bindingof PAF to its receptor (PAFR) is accompanied by ac-tivation of phosphoinositide phospholipase C, leadingto the production of the lipid second messenger andactivation of protein kinase C. There are some similar-ities between PAFR activation and apoptosis inducedby serum deprivation. Identification of the growth fac-tor signal transduction pathways induced by EGb761wouldbeofobviousinterest,forpeptidegrowthfactorshave been implicated in the process of brain develop-ment, neuronal plasticity, survival and repair 23.4. Implications for Alzheimers diseaseThe key feature of neurodegenerative disorders isneuronal cell loss, which leads to a loss of brain tissueand function, which in turn, may manifest as loss ofmemory in Alzheimers disease. While the etiologyofAlzheimersdiseases remainsunknown,a protectivetherapy based on the identification of the mechanismresponsible for cell death may provide an interventionthat slows down or stops progressive neurodegenera-tion. ApplicationofneuroprotectionasthetreatmentofAD has received increasing attention. EGb761, stimu-Y. Luo / Herbal medicine, neuroprotectants, Alzheimers disease405latingthegrowthfactor-mediatedcellsurvivalpathway,wouldhaveprofoundtherapeuticimplicationssincetheproteinaceoustrophicfactors,suchasNGF,donotcrossthe blood-brain barrier as easily as EGb761 does. Al-thoughitisnotuniversallyagreedwhetherthecelldeathin AD is apoptotic or necrotic in nature 45, inhibi-tion of the apoptoticcomponentof neuronaldeath maybe another promising new therapeutic strategy 64.EGb761 has numerous properties, which theoreticallyshould be beneficial in treatment of AD. Its multiplebeneficial actions, including increased blood flow, an-tioxidantactivity,inhibitionofplateletactivatingfactorand nitric oxide, and neuroprotective activity, suggestthat EGb761could be of major therapeutic value in thetreatment of AD. Although that has yet to be proven, ithas already been determined in double-blind, random-ized,placebo-controlledclinicaltrails,thatEGb761hasnomoreadverseeffectsthanplacebotreatment33,34.Pre-clinicalevidencesuggestsanimportantroleforan-tioxidant treatment in protection against free radical-induced neuronal death. This has not yet been con-firmed in clinical trials, but available data are promis-ing 50 and warrant further investigation. If antioxi-dants such as vitamin E and EGb761 are proven effi-cacious in additional AD trials, the simplicity of treat-ment, ease of access, and low cost render these agentsattractive as treatments to delay or slow down the ef-fects of this devastating disorder.It may be that acombination of vitamin E (which is effective at free-radicalscavenging)andEGb761(whichmight bemosteffective at preventing further free-radical production)would be a rational way to use antioxidant therapy inaging and AD. Side effects of high dose use of vita-min E might be attenuated in combined therapy withEGb761.5. ConclusionThe simplicity of treatment, ease of access, and lowcost made Ginkgo biloba extract one of the most pop-ular complementary and alternative medicines for pre-vention and treatment of primary neurodegenerativedementias. In vivo and in vitro experimental evidenceindicates its neuroprotective effects by a “polyvalen-t” action, which may be mediated, at least in part, byanti-oxidative and anti-apoptotic mechanisms. We hy-pothesize that such polyvalent action may have mostefficacious function in preventing oxidative damage inthe cells, presumable by synergistically regulating ox-idative status/balance. Understanding the mechanismsofGinkgobilobaneuroprotectionmaybringaboutnewpossibilities for therapies that exploit multi-leveled,synergistic action against neurodegeneration. Combi-nation therapies, using Ginkgo biloba extracts, repre-sent new avenues for treating neurodegenerative dis-eases such as Alzheimers disease and ameliorate theconsequence of neuronal degeneration in aging.AcknowledgmentsThe author thanks Drs. Peter Butko, Margaret Mc-Donald,andWitoldK.Surewiczforhelpfuldiscussionsand for reading the manuscript.References1B. Ahlemeyer, A. Mowes and J. 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