全 文 ：天然产物研究与开发 NatProdResDev2009, 21:740-743, 765
文章编号:1001-6880(2009)05-0740-05
ReceivedApril21, 2008;AcceptedJune24, 2008
FoundationItem:ThisworkwassupportedbytheNationalNaturalSci-
enceFoundationofChina(20472024, 20772047)andtheNaturalSci-
enceFoundationofGuangdong(04010479, 06025165).
＊CorrespondingauthorTel:86-20-8522-1728;E-mailtliyl@jnu.edu.cn
水团花黄酮类成分及其体外抗病毒活性
李药兰1＊ ,王 辉2 ,范兆永 3 ,苏妙贤 4 ,薛珺一 4 ,李 婷 3 ,岑颖洲 3
1暨南大学药学院中药及天然药物研究所;2暨南大学医学院;3暨南大学生命科学技术学院 ,广州 510632;
4香港中文大学生物系 ,香港 999077
摘 要:从水团花乙醇提物的乙酸乙酯部位分离到 6个黄酮类化合物 , 根据光谱数据分别鉴定为柚皮素(1)、圣
草酚(2)、槲皮素(3)、柚皮素-7-O-β-D-葡萄糖苷(4)、圣草酚-7-O-β-D-葡萄糖苷(5)、槲皮素-3-O-β-D-葡萄糖苷
(6), 化合物 1、2、4和 5为首次从该植物中分离得到。采用细胞病变抑制法(CPEreductionassay)和 MTT法测
定化合物的体外抗病毒活性 , 结果显示 , 三个黄酮苷元 1、2和 3均具有不同程度的体外抑制呼吸道合胞病毒
(RSV)和柯萨奇 B3型病毒(CVB3)活性 ,反之 , 3个黄酮苷均不显示活性。
关键词:水团花;黄酮;抗病毒活性
中图分类号:R284.1;Q946.91 文献标识码:A
FlavonoidsfromAdinapiluliferaandTheirinvitroAntiviralActivity
LIYao-lan1＊ , WANGHui2 , FANZhao-yong3 , SUMiao-Xian4 , XUEJun-Yi4 , LITing3 , CENYing-zhou3
1InstituteofTraditionalChineseMedicine＆NaturalProducts, CollegeofPharmacy, JinanUniversity;2Colegeof
Medicine, JinanUniversity;3DepartmentofChemistry, ColegeofLifeScienceandTechnology, JinanUniversity,
Guangzhou510632 , China;4DepartmentofBiology, theChineseUniversityofHongkong, Hongkong999077 , China
Abstract:SixflavonoidswereisolatedfromtheethylacetatefractionoftheethanolextractofAdinapilulifera.Thechemi-
calstructuresoftheseflavonoidsweredeterminedbyspectroscopicanalysis, andidentifiedtobenaringenin(1), eriodic-
tyol(2), quercetin(3), naringenin-7-O-β-D-glucopyranside(4), eriodictyol-7-O-β-D-glucopyranside(5), andquercetin-
3-O-β-D-glucopyranside(6).Amongthem, compounds1, 2, 4 and5wereisolatedfromA.piluliferaforthefirsttime.An-
tiviraltestsusingcytopathicefect(CPE)reductionassayandMTTmethodrevealedthattheflavonoidaglycones1, 2and
3 possessinvitroantiviralactivityagainstbothrespiratorysyncytialvirus(RSV)andcoxsackieB3 virus(CVB3)todiffer-
entextents.Incontrast, theflavonoidglucosides4, 5and6didnotshowanyanti-RSVandanti-CVB3 efects.
Keywords:Adinapilulifera;flavonoids;antiviralactivity
Introduction
Adinapilulifera(Rubiaceae)isamedicinalplantwidely
distributedinsouthernChinaincludingGuangdong,
Guangxi, Hunan, Fujian, Jiangxi, andZhejiangProv-
inces.Theplanthasbeenusedinfolkmedicinetotreat
variousailmentsincludingcold, fever, andinfectious
diseasesoftherespiratorytract.Theroots, flowers,
fruits, andleavesarethemedicinalyusedpartsofA.
pilulifera[ 1-3] .Phytochemicalstudiesindicatethatthe
plantcontainschromones, chromoneglycosides[ 2] , trit-
erpenoidsandtriterpenoidsaponins[ 3] .However, no
informationisavailableonthepotentialbiologicalac-
tivitiesofphytocompoundsoftheplant.Inthispaper,
wemainlyreportourinvestigationontheisolationof
flavonoidsfromthewholeplantsofA.piluliferaandin
vitroantiviralactivityoftheisolatedflavonoidsagainst
RSVandCVB3infections.
MaterialsandMethods
Plantmaterial
ThewholeplantsofA.piluliferawerecolectedfrom
ShaoguanCounty, GuangdongProvince, ChinainNo-
vember2004, andproperlyauthenticatedbyProf.Bing-
HuiChen(SouthChinaBotanicalGarden, theChinese
AcademyofSciences).Avoucherspecimenwasdepos-
itedforreferenceinthemuseumofSouthChinaBotan-
icalGardenwithaccessionnumberofChenBing-Hui
4766.Thefreshwholeplantscolectedwereairdried
andstoreduntiluseforextraction.
Generalprocedures
HPLC-ESI-MSwasrecordedonaFinniganLCQAd-
vantageMAXinstrument.NMRspectraincluding1H
and13CNMRwereobtainedonaBrukerspectrometer
operatingat300 MHzfor1HMNRand75MHzfor13C
NMR, respectively.Theisolationprocesswasconducted
onsilicagel(200-300meshes, QingdaoHaiyangChem-
icalCo., Ltd., Qingdao, China)column, andsephadex
LH-20(25-100 μm, Fluka, Switzerland)column.TLC
examinationwascariedoutonsilicagelGF254 plates
(0.2 mmthickness, 10×20 cm, Qingdao, China)using
FeCl3 -EtOHreagent, andMolishreagentaschromogen-
icreagents.
Extractionandisolation
DriedandcutwholeplantsofAdinapilulifera(4.7 kg)
weresoakedin95% ethanolatroomtemperaturefor3
times, eachtimefor15 d.Theethanolsolutionswere
thencombined, andconcentratedinvacuumtoyielda
darkgreencrudeextract(570 g).Thecrudeextract
(500 g)wassuspendedindistiledwater(1 L), and
partitionedsuccessivelywithpetroleumether(1 L×
5), ethylacetate(1L×5)andn-butanol(1 L×5).
Afterevaporatedunderreducedpressure, thepetroleum
etherfraction(120 g), ethylacetatefraction(172 g),
n-butanolfraction(185 g), andwaterresiduefraction
(150g)wereobtained, respectively.
Theethylacetatefraction(150g)waschromatographed
onasilicagel(3000 g)columnwhichwaselutedwith
thegradientsolventsystemofpetroleumether:ethylac-
etatetoyieldfoursubfractionsA1 -A4 onthebasisof
theirTLCanalysis.
ThesubfractionA3(28g), whichshowedapositivere-
actiontoFeCl3-EtOHreagent, wasrechromatographed
onasilicagel(1000 g)columnwhichwaselutedwith
thegradientsolventsystemofpetroleumether:ethylac-
etatetoyieldsevensubfractionsA3-1-A3-7.Thesubfrac-
tionA3-2(480 mg)wasfurtherisolatedonasilicagel
(20 g)columnwhichwaselutedwithn-hexane:ace-
tone(7∶3)folowedbyasephadexLH-20columnwhich
waselutedwithchloroform:methanol(9∶1)toyield
compound1(12 mg).ThesubfractionA3-3 (970 mg)
wasfurtherisolatedonasilicagel(35g)columnwhich
waselutedwithn-hexane:acetone(7∶3)folowedbya
sephadexLH-20 columnwhichwaselutedwithchloro-
form:methanol(9∶1)toyieldcompound2(7mg)and3
(8 mg).
ThesubfractionA4(15 g), whichshowedapositivere-
actiontoFeCl3 -EtOHreagent, wasrechromatographed
onasilicagel(600 g)columnwhichwaselutedwith
thegradientsolventsystemofchloroform:methanolto
obtainfoursubfractionsA4-1 -A4-4.ThesubfractionA4-1
(3.5g)wasfurtherisolatedonasilicagel(110g)col-
umnwhichwaselutedwithn-hexane:acetone(7∶3)fol-
lowedbyasephadexLH-20 columnwhichwaseluted
withchloroform:methanol(9∶1)toyieldcompound3(3
mg).ThesubfractionA4-2(4.3 g)wasfurtherisolated
onasilicagel(150 g)columnwhichwaselutedwith
thegradientsolventsystem ofchloroform:methanol,
andthenrepeatedlypurifiedwithasephadexLH-20
columnwhichwaselutedwithchloroform:methanol(7
∶3)toyieldcompound4(10 mg)and5(12 mg).The
subfractionA4-3(6.7 g)wasfurtherisolatedonapoly-
amidecolumnwhichwaselutedwiththegradientsol-
ventsystemofchloroform:methanol, andthenrepeated-
lypurifiedwithasephadexLH-20 columnwhichwas
elutedwithchloroform:methanol(7∶3)toyieldcom-
pound6(12 mg).
Celsandviruses
HEp-2 cels(Humanlarynxepidermoidcarcinoma
cels), HeLacels(Humancervicalcarcinomacels),
RSV(Longstrain), andCVB3 werekindlyprovidedby
Prof.YifeiWangoftheBiomedicalResearch＆Devel-
opmentCenter, JinanUniversity, Guangzhou, China.
HEp-2 celsandHeLacelswereusedforculturing
RSVandCVB3 inthisexperiment, respectively.The
celsweregrowninEagle sminimumesentialmedi-
um(MEM)(Gibco)supplementedwith10% fetalbo-
vineserum(FBS)(Gibco), 25μg/mLgentamicin(Sig-
ma)and200 mML-glutamine(Sigma)(growthmedi-
um).Virus-infectedcelsweremaintainedinMEM
with1% FBS, 25 μg/mLgentamicinand200 mML-
741Vol.21 LIYao-lan, etal:FlavonoidsfromAdinapiluliferaandTheirinvitroAntiviralActivity
glutamine(maintenancemedium).Althecelswere
culturedat37 ℃ inahumidifiedatmospheresupplied
with5%CO2.Virustitersweredeterminedbythe50%
tissuecultureinfectivedose(TCID50)method.
Cytotoxicityassay
CelularviabilitywasassayedwiththeMTTmethodu-
singatetrazoliumsalt(3-[ 4, 5-dimethylthiazol-2-yl] -
2, 5-diphenyltetrazoliumbromide)asdescribedinour
previousreport[ 4] .Inbrief, serialydilutedconcentra-
tionsofsamples(100 μL)wereappliedtothewelsof
96-welplatecontainingconfluentcelmonolayerin
triplicate, whilethedilutionmediumwithoutthesam-
pleswasusedasthecontrol.After2 dofincubation,
MTTsolution[ 5 mg/mLinphosphatebuferedsaline
(PBS)] wasadded tothewelstoform MTT
formazan.Theopticaldensity(OD)wasreadatamicro-
platespectrophotometeratdoublewavelengthsof540
and 690 nm.Themedian cytotoxicconcentration
(CC50)wascalculatedastheconcentrationofthesam-
plethatdecreasedthenumberofviablecelsto50%of
thecelcontrolthroughtheODvaluesofviablecelsin
comparisonwithnon-viablecels.Themaximalnon-cy-
totoxicconcentration(MNCC)wasdeterminedasthe
maximalconcentrationofthesamplethatdidnotexert
toxicefect.
Antiviralassay
Thecytopathicefect(CPE)reductionassaydescribed
inourpreviousreport[ 4] wasusedtodeterminethean-
tiviralactivitiesofsamplesagainstRSVandCVB3.In
brief, toconfluentmonolayerofcelsin96-welmicroti-
treplate, 50 μLofvirussuspensioncontaining100
TCID50 and50 μLofmaintenancemediumcontaining
appropriateserialydilutedconcentrationsofthesam-
pleswereadded.MNCCofthetestsamplewasusedas
thehighestconcentrationfromwhichaserialtwofold
dilutionwasmadewiththeculturemedium.Ribavirin
wasruninparalelasthepositivecontrolinbothanti-
RSVandanti-CVB3 tests.Toactasviruscontroland
celcontrol, thevirussuspensionandmaintenanceme-
diumwithoutsampleswereadded, respectively.The
concentrationthatreduced50% ofCPEinrespectto
thatofviruscontrolwasestimatedfromtheplotsofthe
dataandwasdefinedas50% inhibitoryconcentration
(IC50).Theselectivityindex(SI)wascalculatedfrom
theratioofCC50 toIC50.
ResultsandDiscussion
Identification
Duetotheantiviralefectoftheethylacetatefractionof
theethanolextractofA.pilulifera(preliminaryscreen-
ing, nodatashown), theethylacetatefractionwasfur-
therseparatedwithcolumnchromatography, leadingto
obtainsixpurecompounds.Chemicalreactionsexhibi-
tedthataloftheisolatedcompoundswerepositiveto
FeCl3-EtOHreagent, andcompounds4, 5 and6 were
alsopositivetoMolishreagent.Theirchemicalstruc-
tureswerefinalyidentifiedtobenaringenin(1), eriod-
ictyol(2), quercetin(3), naringenin-7-O-β-D-glucopy-
ranside(4), eriodictyol-7-O-β-D-glucopyranside(5),
andquercetin-3-O-β-D-glucopyranside(6)byspectro-
scopicanalysisandcomparisonwiththeirpublishedda-
ta[ 5-9] .Amongthem, compounds1, 2 andtheirgluco-
sides4, 5 wereisolatedfromA.piluliferaforthefirst
time.
Naringenin(1) Yelow powder, waspositiveto
FeCl3-EtOHreagent.PositiveLC-ESI-MSm/z:273 [ M
+H] +;1HNMR(CD3OD)δ:7.30(2H, d, J=8.7
Hz, H-2′, 6′), 6.81(2H, d, J=8.7 Hz, H-3′, 5′),
5.89 (1H, d, J=2.1 Hz, H-8), 5.87(1H, d, J=2.1
Hz, H-6), 5.34(1H, dd, J=12.9, 3.0 Hz, H-2), 3.14
(1H, dd, J=17.1, 12.9 Hz, H-3b), 2.70(1H, dd, J
=17.1, 3.0 Hz, H-3a);13 CNMR(CD3OD)δ:197.8
(C-4), 168.3(C-7), 165.5(C-5), 164.9(C-9),
159.0(C-4′), 131.1(C-1′), 129.0(C-2′, 6′), 116.3
(C-3′, 5′), 103.3 (C-10), 97.0(C-6), 96.1(C-8),
80.5(C-2), 44.0(C-3).
Eriodictyol(2) Yelowpowder, waspositiveto
FeCl3-EtOHreagent.PositiveLC-ESI-MSm/z:311 [ M
+Na] + , 289 [ M+H] +;1HNMR(CD3OD)δ:6.86
(1H, s, H-2′), 6.73(2H, s, H-5′, 6′), 5.85(1H, d, J
=2.1Hz, H-8), 5.83(1H, d, J=2.1Hz, H-6), 5.26
(1H, dd, J=12.9, 3.0 Hz, H-2), 3.08(1H, dd, J=
17.2, 12.9 Hz, H-3b), 2.68(1H, dd, J=17.2, 3.0
Hz, H-3a);13CNMR(CD3OD)δ:197.7(C-4), 168.4
(C-7), 165.4(C-5), 164.8(C-9), 146.8(C-4′),
146.5(C-3′), 131.8(C-1′), 119.2(C-6′), 116.3(C-
742 NatProdResDev Vol.21
5′), 116.2 (C-2′), 103.3(C-10), 97.0(C-6), 96.2
(C-8), 80.5(C-2), 44.1(C-3).
Quercetin(3) Yelowpowder, waspositivetoFeCl3-
EtOHreagent.PositiveLC-ESI-MSm/z:325 [ M+
Na] + , 303 [ M+H] +;1HNMR(CD3OD)δ:7.72
(1H, d, J=2.1Hz, H-2′), 7.64(1H, dd, J=8.4, 2.1
Hz, H-6′), 6.88(1H, d, J=8.4 Hz, H-5′), 6.38(1H,
d, J=2.1Hz, H-8), 6.17(1, d, J=2.1 Hz, H-6);13C
NMR(CD3OD)δ:177.4(s, C-4), 165.6(s, C-7),
162.5(d, C-9), 158.2(s, C-5), 148.8(s, C-4′),
146.2(s, C-2), 145.7(s, C-3′), 137.2(s, C-3),
124.1(s, C-1′), 121.7(d, C-6′), 116.2(d, C-5′),
115.7(d, C-2′), 104.1(s, C-10), 99.2(d, C-6), 94.4
(d, C-8).
Naringenin-7-O-β-D-glucoside(4) Yelowpowder,
waspositivetobothFeCl3 -EtOHreagentandMolishre-
agent.PositiveLC-ESI-MSm/z:457 [ M+Na] +, 435
[ M+H] +, 273.2[ M+H-162] +;1HNMR(CD3OD)
δ:7.27(2H, d, J=8.4 Hz, H-2′, 6′), 6.77(2H, d, J
=8.7 Hz, H-3′, 5′), 6.16(1H, s, H-8), 6.14(1H, s,
H-6), 5.35(1H, dd, J=12.9, 2.7 Hz, H-2), 4.93
(1H, d, J=7.0, H-1″), 3.14(1H, dd, J=17.1, 12.9
Hz, H-3b), 2.71(1H, dd, J=17.1 , 2.7 Hz, H-3a);
13CNMR(CD3OD)δ:198.9(C-4), 166.5(C-7),
164.3(C-5), 164.1(C-9), 158.1(C-4′), 130.6(C-
1′), 129.1(C-2′, 6′), 116.4(C-3′, 5′), 104.7(C-
10), 100.6(C-1″), 97.9(C-6), 96.9(C-8), 80.2(C-
2), 77.6(C-3″), 77.1(C-5″), 74.1(C-2″), 70.6(C-
4″), 61.8(C-6″), 43.4(C-3).
Eriodictyol-7-O-β -D-glucoside(5) Yelowpowder,
waspositivetobothFeCl3 -EtOHreagentandMolishre-
agent.PositiveLC-ESI-MSm/z:473[ M+Na] +, 451
[ M+H] +, 289[ M+H-162] +;1HNMR(CD3OD)δ:
6.91(1H, s, H-2′), 6.78(2H, s, H-5′, 6′), 6.20(1H,
d, J=1.8 Hz, H-8), 6.18(1H, d, J=1.8 Hz, H-6),
5.33(1H, d, J=12.6, 2.7 Hz, H-2), 4.97(1H, d,
7.0, H-1″), 3.13(1H, dd, J=17.1, 12.6 Hz, H-3b),
2.76(1H, dt, J=17.1, 2.7 Hz, H-3a);13 CNMR
(CD3OD)δ:198.5(C-4), 167.0(C-7), 164.9 (C-
5), 164.5(C-9), 146.9(C-4′), 146.5(C-3′), 131.5
(C-1′), 119.3(C-6′), 116.2(C-5′), 114.8(C-2′),
104.9(C-10), 101.2(C-1″), 98.0(C-6), 96.9(C-
8), 80.7(C-2), 78.2(C-3″), 77.8(C-5″), 74.6(C-
2″), 71.1(C-4″), 62.3(C-6″), 44.0(C-3).
Quercetin-3-O-β-D-glucoside(6) Yelowpowder,
waspositivetobothFeCl3-EtOHreagentandMolishre-
agent.PositiveLC-ESI-MSm/z:487 [ M+Na] + , 465
[ M +H] +, 303.0 [ M +H-162 ] +;1H NMR
(CD3OD)δ:7.66(1H, d, J=2.1 Hz, H-2′), 7.54
(1H, dd, J=8.4 , 2.1 Hz, H-6′), 6.82(1H, d, J=8.4
Hz, H-5′), 6.35(1H, d, J=2.1 Hz, H-8), 6.16(1H,
d, J=2.1 Hz, H-6), 5.22(1H, d, J=7.5 Hz, H-
1″);13CNMR(CD3OD)δ:179.3(C-4), 166.0(C-7),
162.8(C-5), 158.9(C-9), 158.3(C-4′), 149.8(C-
2), 145.8 (C-3′), 135.6(C-3), 123.2(C-1′), 123.0
(C-6′), 117.6(C-5′), 116.0(C-2′), 105.5(C-10),
104.4(C-1″), 99.9(C-6), 94.8(C-8), 78.2(C-3″),
78.0(C-5″), 75.7(C-2″), 71.1(C-4″), 62.5(C-6″).
Antiviralactivity
Inthepresentinvestigation, CPEreductionassayand
MTTmethodwererespectivelyusedtotesttheantiviral
activityandcytotoxicityoftheisolatedcompounds, and
theSIvaluecalculatedfromtheratioofCC50 toIC50
wasusedasanimportantparametertoevaluatethean-
tiviralactivityofthetestedsamples.Asaresult, three
flavonoidaglycones3, 2 and1 possessantiviralactivi-
tiesagainstRSVwithIC50 valuesof2.5 , 6.3, and23.5
μg/mL, andselectivityindex(SI)valuesof>200,
10.2 and2.9, andagainstCVB3 withIC50 valuesof
15.7, 31.3 and31.3 μg/mL, andSIvaluesof>31.8,
8.4, and2.7, respectively.Ofthethreeflavonoidagly-
cones, quercetin(3)comprisingmosthydroxylgroupsin
itsstructureappearstobethemostpotentantiviralac-
tivityagainstbothRSVandCVB3.Incontrast, three
flavonoidglucosides4, 5 and6 donotshowanyanti-
RSVandanti-CVB3 efects.Therefore, theactivemoie-
tyresponsiblefortheantiviralactivityofflavonoids
maybetheflavonoidaglycone, andthenumbersofhy-
droxylgroupslinkedintheaglyconeskeletonseemto
beimportantfortheantiviralactivityofflavonoids.
References
1 FanGJ, HeZS.Generalintroductionofthestudiesonthe
chemicalconstituentsofAdinaplant.ForeignMedicalSci-
ences:TCMSection, 1996, 18:12-14.
(下转第 765页)
743Vol.21 LIYao-lan, etal:FlavonoidsfromAdinapiluliferaandTheirinvitroAntiviralActivity
伐他汀和 STT各剂量均能降低 ICAM-1和 VCAM-1
基因的表达(P<0.01 ～ P<0.05),并增加 PPARα、
PPARγ基因表达(P<0.01)。所以我们同时推测 ,
可能的原因是:首先 , STT直接作于 VCAM-1、
ICAM-1、PPARα和 PPARγ靶基因 。其次 , STT减少
NF-κB激活 ,随之 PPARα、PPARγ基因的激活抑制
了 VCAM-1和 ICAM-1基因的表达 ,或者同时是 NF-
κB信号转导通路的抑制降低了 NF-κB依赖性致炎
基因 ICAM-1和 VCAM-1的表达 。
STT使血管壁 ICAM-1、VCAM-1基因低表达和
PPARα、PPARγ基因的激活 ,减轻了动脉粥样硬化
发生的炎症作用 ,延缓了动脉粥样硬化的发展 。揭
示 STT对 ICAM-1、VCAM-1基因下调和对 PPARα、
PPARγ基因的上调作用 ,可能是 STT抗动脉粥样硬
化作用机制之一 。
参考文献
1 HuangZH(黄震华).Efectsofangiotensinconvertingen-
zymeinhibitoronatherosclerosis.ForeignMedicalSciences:
SectionofInternalMedicine(国外医学 , 内科学分), 2003,
30(3):93-95.
2 NiuW(牛伟).EfectofSaponinfromTribulusterrestrisL.
onmetabolicsyndromeandanalysisofitsfunctionalcompo-
nents.Shanghai:EastChinaNormalUniversity(华东师范大
学), 2005.
3 LiJG(李家贵).EffectandmolecularmechanismsofSapo-
ninfrom TribulusterrestrisL.onlipidmetabolicdisorder
mice.Shanghai:EastChinaNormalUniversity(华东师范大
学), 2007.
4 ZhangY(张颖), ZhangB(张波), etal.EffectofGSTTon
hyperlipemiaandearlyatheroscleroticlesionofaorticintima
inrabbits.ChinJIntegrMedCardio/CerebrovascDis(中西
医结合心脑血管病杂志), 2006, 4:126-128.
5 YinHJ(殷惠军), ZhangB(张波), ShiDZ(史大卓), etal.
EfectsofGTSSonexpressionofNF-κB, ICAMandTNF-α
inatheroscleroticrabbits.ChinJIntegrMedCardio/Cerebro-
vascDis(中西医结合心脑血管病杂志), 2005, 3:700-702.
6 YangPY(杨鹏远), RuiYC(芮耀诚), etal.Establishment
ofexperimentalatherosclerosismodelinrats.AcadJSecMil
MedUniv(第二军医大学报), 2003, (7):802-804.
7 HuJT(胡建廷).Cilostazolamelioratedexpressionofadhe-
sionmoleculesintheretinaofstz-induceddiabeticrats:Pos-
sibleviappars.Shandong:ShandongUniversity(山东大学),
2005.
8 ZhangYM(张玉梅), LiuY(刘颖), etal.Soyisflavonesin-
hibitsgeneexpressionofintercellularadhesionmolecule-1
andvascularceladhesionMolecule-1 inaortavesselofath-
eroscleroticrat.ChinJArter(中国动脉杂志), 2003, 11:13-
16.
9 TanakaT, ItohH, DoiK, etal.Downregulationofperoxi-
someproliferator-activatedreceptorγexpressionbyinflamma-
torycytokinesanditsreversalbythiazolidinediones.Diabeto-
logia, 1999, 42:702-710.
10 BensonSC, HoCI, etal.Identificationoftelmisartanasau-
niqueangiotensin IIreceptorantagonistwith selective
PPARγmodulatingactivity.Hypertension, 2004, 43:661-666.
11 DeleriveP, GerviosP, etal.InductionofIκBαexpressionas
amechanismcontributingtotheanti-inflammatoryactivities
ofPPARαactivators.JBiolChem, 2000, 275:36703-36707.
12 YinHJ(殷惠军), ZhangP(张波), ShiDZ(史大卓).
EfectsofGTSSonexpressionofNF-κB, ICAMandTNF-α
inatheroscleroticrabbit.ChinJIntegrMedCardio/Cerebro-
vascDis(中西医结合心脑血管病杂志), 2005, 3:700-702.
(上接第 743页)
2 GuoYW, HuangWH, SongGQ, etal.Chemicalshiftassign-
mentoftwochromoneglycosidesextractedfromChineseherb
Adinapilulifera.ChinJMagnReson, 2003, 20:265-269.
3 ShiHM, MinZD.TwonewtriterpenoidsaponinsfromAdina
pilulifera.JAsianNatProdRes, 2003, 5:11-16.
4 LiYL, ButPPH, OoiVEC.Antiviralactivityandmodeofac-
tionofcaffeoylquinicacidsfromScheffleraheptaphylla(L.)
Fordin.AntiviralRes, 2005, 68:1-9.
5 RenDM, LouHX, JiM.StudiesonconstituentsofDacoceph-
alumrupestra.ChinPharmJ, 2005, 40:1695-1696.
6 ZhangCG, LiBG, GuJ, etal.ChemicalstudyonExbuck-
landiapopulnea.NatProdResDev(天然产物研究与开
发), 2003, 15:308-309.
7 YangJ, etal.StudiesonchemicalconstituentsofBerchemia
polyphyllavar.leioclada.ChinPharmJ, 2006, 41:255-257.
8 YangH, SungSH, KimYC.Twonewhepatoprotectivestil-
beneglycosidesfromAcermonoleaves.JNatProd, 2005,
68:101-103.
9 YuDQ, YangJS.TheHandbookofAnalyticalChemistry,
NMRSection, 2nd Ed.Beijing:ChemicalIndustryPress,
1999.822.
765Vol.21 石昌杰等:蒺藜皂苷对动脉粥样硬化大鼠动脉壁 ICAM-1、VCAM-1、PPARα、PPARγ基因表达的影响