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FoodScienceandHumanWellness
食品科学与人类健康(英文)
ISSN2213-4530,CN10-1750/TS
《FoodScienceandHumanWellness》网络首发论文
题目:2-O-β-D-Glucopyranosyl-L-ascorbicacid,anascorbicacidderivativeisolated
fromthefruitsofLyciumbarbarumL.,ameliorateshighfructose-induced
neuroinflammationinmice:involvementofgutmicrobiotaandleakygut
作者:WeiDong,YujiaPeng,GuijieChen,ZhiyongXie,WeiqiXu,WangtingZhou,
JiaMi,LuLu,YiSun,XiaoxiongZeng,YoulongCao,YameiYan
收稿日期:2022-02-09
网络首发日期:2022-08-31
引用格式:WeiDong,YujiaPeng,GuijieChen,ZhiyongXie,WeiqiXu,WangtingZhou,
JiaMi,LuLu,YiSun,XiaoxiongZeng,YoulongCao,-O-β
-D-Glucopyranosyl-L-ascorbicacid,anascorbicacidderivativeisolatedfromthe
fruitsofLyciumbarbarumL.,ameliorateshighfructose-induced
neuroinflammationinmice:involvementofgutmicrobiotaandleaky
gut[J/OL].FoodScienceandHumanWellness.
.
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版广电总局批准的网络连续型出版物(ISSN2096-4188,CN11-6037/Z),所以签约期刊的网络版上网络首
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:.
Publishedonlineꎺ2022-08-3109:37:59
URLꎺ.
./FoodScienceandHumanWellness13(2024)
ContentslistsavailableatCNKI
FoodScienceandHumanWellness
journalhomepage:-science-and-human-wellness
2-O-β-D-Glucopyranosyl-L-ascorbicacid,anascorbicacidderivativeisolated
fromthefruitsofLyciumbarbarumL.,ameliorateshighfructose-induced
neuroinflammationinmice:involvementofgutmicrobiotaandleakygut
WeiDonga,YujiaPenga,GuijieChena,ZhiyongXiea,WeiqiXua,WangtingZhoua,JiaMib,c,
LuLub,c,YiSuna,XiaoxiongZenga*,YoulongCaob,c*,YameiYanb,c*
aCollegeofFoodScienceandTechnology,NanjingAgriculturalUniversity,Nanjing210095,Jiangsu,China
bInstituteofWolfberryEngineeringTechnology,NingxiaAcademyofAgricultureandForestrySciences,Yinchuan,750002,Ningxia,China
cNationalWolfberryEngineeringResearchCenter,Yinchuan750002,Ningxia,China
ABSTRACT:Westerndiet(richinhighlyrefinedsugarandfat)caninducearangeofmetabolicdysfunctionsin
animalsandhumans,
impairment,twocriticalpathologicalcharacteristicsofAlzheimer’sdisease,havebeencloselyassociatedwith
microbialalterationviathegut-,thepresentstudyaimedtoinvestigatetheinfluenceof
2-O-β-D-glucopyranosyl-L-ascorbicacid(AA-2βG)isolatedfromthefruitsofLyciumbarbarumonpreventingthe
high-fructosediet(HFrD)-2βGpreventedHFrD-induced
-2βGalsopredominantlyenhancedthegutbarrierintegrity,decreasedlipopolysaccharideentry
intothecirculation,
beneficialeffectsweretransmissiblebyhorizontalfecalmicrobiometransplantation,transferringfromAA-2βGfed
,AA-2βGexertedneuroprotectiveeffectsinvolvingtheenrichmentof
LactobacillusandAkkermansia,
AA-2βGcouldimproveindicesofcognitionandneuroinflammmationviamodulatinggutdybiosisandpreventing
,AA-2βGmaybeappliedtoattenuateneuroinflammation
associatedwithWestern-stylediets.
Keywords:Neuroinflammation;Gutmicrobiota;Leakygut;Lipopolysaccharide;Fecalmicrobiometransplantation;
2-O-β-D-Glucopyranosyl-L-ascorbicacid

Totalfructoseconsumptionhasdrasticallyincreasedduetotheextensivecommercialuseof
high-fructosecornsyrup(HFCS)assweetenersforbeverages,snacksandbakedgoods[1].Accumulating
evidencedemonstratedthatfructosecouldinduceinflammatoryresponsesinperipheraltissues,andattention
hasalsobeenpaidontheabilityofthissugartoinduceneuroinflammation[2].Neuroinflammationisa
pathologicalhallmarkofneurodegenerativedisease,includingAlzheimer’sdisease(AD)[3].AD,an
increasinglycommonneurodegenerativedisease,afflictsmorethan50millionpeopleworldwide[4].Italso
*CorrespondingauthorReceived9February2022
******@();******@();Receivedinrevisedfrom25March2022
******@()Accepted7April2020
:.
./FoodScienceandHumanWellness13(2024)
drasticallyimpairsindividual’squalityoflifeandincreaseshealthcarecost,whichhasbecomesocialproblem
[5].However,thereisnospecificdrugtocureeffectivelythediseaseorreversetheprocessofdisease.
Therefore,itneedstoconsidervaluableapproachestopreventADbasedonvariouspathologicalpathways.
Inrecentyears,accumulatingevidenceindicatesthatgutmicrobiotacaninfluencethecentralnervous
system(CNS)throughthegut-brainaxis,subsequentlymodulatingthebrainfunctionandhostbehavior[6].
Forinstant,recentworkindicatedacausativerelationshipbetweenthegutmicrobiotaandthedevelopmentof
cognitivedeficitswithtransferabilityofphenotypesviafecalmicrobiotatransplantation(FMT)[7].For
another,thediet,asoneoftheimportantmediatorsofgutmicrobiota,hasanimpactonneurodegenerative
disease[6].Ofnote,ampleevidenceindicatesthatthecognitivedeclinesandneuroinflammationinducedby
Westerndietseemtobemediated,atleastpartly,bygutmicrobiota[8].Specifically,otherstudieshaveshown
thathigh-fructosediet(HFrD)couldalterthemicrobialcompositionandincreasegutpermeability,which
exacerbatedtheleakageoflipopolysaccharide(LPS)intothebloodcirculation[9,10].IncreasedaccessofLPS
intothecirculationcouldfurthertriggertheneuroinflammationprocess,subsequentlycontributingto
cognitiveimpairment[9].Inlinewiththis,theadministrationofperipheralLPScouldaggravatetheactivation
ofastrocytesandmicroglia,elevatingthelevelsofpro-inflammatoryfactorsinthebrain[11].Hence,gut
dysbiosismaybeanunderlyingriskfactorinneuroinflammation,cognitivedeficiencyandrelateddiseases.
Consequently,developingasafe,effectiveandeasilyimplementaldiet-mediatedinterventionstrategythatcan
altergutmicrobiotawillbeveryimportanttopreventordelaytheprogressionofAD.
LyciumbarbarumL.,asatonicfoodandtraditionalChinesemedicine,hasbeendemonstratedtohave
variousbiologicalfunctionsincludinganti-tumor,anti-inflammatory,immunomodulatoryand
neuroprotectiveactivities[12].Specifically,ithasbeenprovedbybothcellandanimalmodelsthatL.
barbarumcanexertdirectneuroprotectiveeffectsonneuronaldiseases,includingAD,Parkinson’sdisease
andothertypicalneurodegenerativediseases[13].Asastableascorbicacid(AA)derivativefirstlyseparated
,thecontentof2-O-β-D-glucopyranosyl-L-ascorbicacid(AA-2βG)isabout
%[14].IthasbeenreportedthatAA-
exhibitedantioxidant,anti-tumorandimmunomodulatoryeffects[15-17].Inaddition,wepreviouslyreported
thatAA-2βGcouldreducetheinflammationindextransodiumsulfate-inducedcolitismicebydecreasing
endotoxin,enhancingtheintestinalpermeabilityandmodulatingthegutmicrobiota[18].However,the
possibilitythatwhetherAA-2βGcanattenuateneuroinflammationandcognitivedeficitshasnotbeen
,wehypothesizedthatAA-2βGprotectedagainstneuroinflammationbyremodelingofthegut
-2βGamelioratedintestinalbarrierdefect,
reducedserumLPS,suppressedglialcellsactivationandneuroinflammation,andultimatelyalleviated
,manifestingthat
thegutmicrobiomemediatedtheneuroprotectioneffectsproducedbyAA-
thatAA-2βGpossiblycontributedtotheinhibitionofhippocampalneuroinflammationinHFrD-fedmice.
:.
./FoodScienceandHumanWellness13(2024)

-2βG
AA-2βG(purity>90%)()providedby
theNationalWolfberryEngineeringResearchCenter(Yinchuan,China).Themethodofpreparation(see
SupplementaryMaterialsandMethods)wasdescribedindetailinourpreviousstudy[18].


C57BL/6(7weeksold)malemice((20±1)g,averagebodyweight(bw))werepurchasedfromShanghai
SLACLaboratoryAnimalCo.,Ltd.(Shanghai,China).Allthemicewerehousedinaspecificpathogen-free
(SPF)condition(SYXK-<Jiangsu>-2011-0037,Nanjing,China)under12/12dark-
was(50±5)%andambienttemperaturewas(25±2)℃.

TheexperimentswereapprovedbytheGuidelinesoftheEthicalCommittee
(SYXK-<Jiangsu>-2011-0037,Nanjing,China)ofNanjingAgriculturalUniversity(Approvalno.
PZ2020089).
:ExperimentalschemeforHFrD-inducedneuroinflammationandcognitivedeficitsin
mice
Micethatacclimatedfor1weekwereallocatedto3groups(n=13pergroup)andtreatedasfollows(Fig.
1A):Thecontrolmice(NCgroup)werefedwithanormaldiet(starch(%)andsucrose(%))for8
(HFrDgroup)werefedwithHFrD(starch(%),sucrose(1%)andfructose(%),
JiangsuSynergyPharmaceuticalBiologicalEngineeringCo.,Ltd,Nanjing,China)
resultsofourpreviousresearch[18],150mg/(kg·d)ofAA-2βGdosagewaschoseninrodentmodelsfroma
,themicewerefedwithHFrDandtreatedwithAA-2βG(AAgroup)at150
mg/(kg·d)byintragastricgavagefor8weeks(200μLpermice).
:.
./FoodScienceandHumanWellness13(2024)
-2GalleviatescognitiveimpairmentandneuroinflammationinHFrD-fedmice.(A)Schemeofanimal
experiment.(B)Representativeswimmingpathsofmice.(C)Meanlatency(sec)toreachplatformduringtrainingsessionof
MWM(*P<).(D)ThenumberofcrossingsduringtheprobetestofMWM.(E)Thepercentageofdistanceinthetarget
quadrant(wheretheplatformwaslocatedduringtrainingsession)duringtheprobetestofMWM.(F)Thepercentageoftime
spentinthetargetquadrant.(G)LPS,TNF-,IL-6,andIL-10levels(n=5-8).(H)RepresentativephotomicrographsofH&E
stainingofhippocampalDG,CA1,andCA3region,andcortex(scalebar,50m),bottomleftcornerofeachimage
representativehighermagnificationimage.(I)TheimmunofluorescentstainingofIba-1andGFAPinDGandCAofthe
hippocampus(n=3,200×magnification).ThemeandensityoftheIba-1andGFAPwasanalyzedbyImageJsoftware.
TNF-,IL-1,IL-6,iNOS,MCP-1,TLR4,NLRP3andMyD88mRNAlevelsinthehippocampus(J)andcortex(K)(n=6).
Significantlydifferences:differentletters,P<-wayANOVA.
:FMT
Therecipientmice(n=13pergroup)werefedHFrDandtreateddailywithtransplantmaterialfrom
eitherHFrD-fedmiceorAA-2βG-fedmice(animalprotocol1)for8weeks().FMTwasperformed:.
./FoodScienceandHumanWellness13(2024)
andslightlymodifiedbasedonthepreviousreport[19].Freshfecalpelletsampleswerecollectedfrom
(400
mgstoolsdissolvedin4mLsterilesaline).FMTgroupsoffecalslurrywerecentrifugedat4℃(1000r/min)
,thecollection
offecalsupernatantandoralgavage()werecompletedwithin15min.
:Intestinalpermeabilityexperiment
Inanimalprotocol1andanimalprotocol2,threemicefromeachgroupwereusedforexperimentof
(FITC)-dextranpermeabilityassaywasusedto
assessintestinalpermeabilityasdescribedpreviously[10].Briefly,allanimalsfastedfor4hwere
administeredFITC-dextr