全 文 ：海南砂仁挥发油对实验性溃疡性结肠炎小鼠抗氧化和抗 NO自由基作
用(英文)
赵　锦 1 , 　朱　毅 1＊ , 　董　志2 , 　陈国彪 1 , 　刘　春 1
(1.海南省药品检验所 ,海南 海口 570216;2.重庆医科大学药学院药理教研室 ,重庆市生物化学及分子药理
学重点实验室 ,重庆 630000)
Foundation:Supportedby2007NationalKeyTechnologyR＆Dprogram(2007BAI27B06);2006KeyScienceandTechnologyProjectsofHainan
Province(06207)
Introductiontoauthor:ZHAOJin(1983-), female, masterofpharmacology.Email:zhaojin200711@ 163.comTel:13118915047.
Correspondenceto:Prof.ZHUYi, doctorofpharmacology, thetutorofdoctor.Email:hnzhuyi@ 126.comTel:0898-66832901
关键词:海南砂仁;挥发油;溃疡性结肠炎;抗氧化;NO;iNOS;DSS;小鼠
摘要:目的:考察海南砂仁挥发油的抗氧化及抗 NO作用 , 对海南砂仁挥发油抗实验性溃疡性结肠炎(UC)作用机制进行
初步探讨。方法:自由饮用 4%右旋葡聚糖硫酸钠(DSS)溶液建立 UC模型。生化法测定正常对照组 、模型对照组 、海南
砂仁挥发油高 、中 、低剂量组及 SASP阳性药对照组小鼠肠组织中 SOD、MDA以及 NO水平;免疫组化考察各组的 iNOS
表达。结果:海南砂仁挥发油中高剂量给药可以显著降低模型组肠组织中 MDA水平 , 显著升高 SOD水平 , 并且可显著
降低模型小鼠 NO及 iNOS水平。结论:海南砂仁挥发油具有抗氧化及抗 NO作用 , 其可通过抑制 iNOS表达 ,减少 NO过
量生成 , 是海南砂仁挥发油发挥抗 UC的作用机制之一。
中图分类号:R285.6　　　　　文献标识码:A　　　　　文章编号:1001-1528(2009)09-1334-05
AntioxidativeandantinitrosativeeffectsofvolatileoilfromA.longiligulareT.L.
Wuonulcerativecolitismice
ZHAOJin1 , 　ZHUYi1＊ , 　DONGZhi2＊ , 　CHENGuo-biao1 , 　LIUChun1
(1.HainanProvincialInstituteforDrugControl, Haikou570216, China;2.DepartmentofPharmacology, ChongqingMedicalUniversity, Biochemistry
andMolecularPharmacologyKeyLaboratory, Chongqing630000 , China)
KEYWORDS:A.longiligulareT.L.Wu;volatileoil;ulcerativecolitis;antioxidation;NO;iNOS;DSS, mouse
ABSTRACT:AIM:ToinvestigateantioxidativeandantinitrosativeefectsofvolatileoilfromA.longiligulareT.L.
Wuondextransulfatesodium(DSS)-inducedulcerativecolitismice.METHODS:Balb/cmicewerefedwith4%
DSSsolutionfor7 dtoinduceulcerativecolitis.Usingbiochemicalmethod, theactivityofantioxidativeenzyme
SOD, MDAandNOweredeterminedinnormal, model, SASPandthreemouse sgroupswithlow, moderateand
highvolatileoilfromA.longiligulareT.L.Wurespectively.Atthesametime, theactivityofiNOSwasalsomeas-
uredbyimmunohistopathology.RESULTS:TheconcentrationofMDAandNOwerereducedandSODincreased
significantlyinhigh-andmoderate-volatileoilgroupscomparedwiththoseinthemodelgroup.TheactivityofiNOS
wasreducedsignificantlyinhigh-andmoderate-volatileoilgroupscomparedwiththoseinthemodelgroup.There-
sultsdemonstratedthattheexpressionofiNOSwassignificantlyinhibitedinDSS-inducedulcerativecolitismiceaf-
terbeingtreatedwithhighormoderate-dosagevolatileoil.CONCLUSION:VolatileoilfromA.longiligulareT.L.
WuhasantioxidativeandantinitrosativeefectswhichmaybeoneofthemechanismfortreatingUC.
　　AmomiSemen, adryripefruitofA.vilosum
Lour., A.longiligulareT.L.Wu, orA.ilosumLour.
var.xanthioidesT.L.WuetSenjen, belongstoZingib-
eraceae.ItisXin(pungent)andWen(Warm)with
thefunctionsofeliminatingdampandimprovingappe-
tite, warmingthespleen, checkingdiarhea, regula-
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tingqi-flowingandpreventingabortion[ 1] .Ulcerative
colitis(UC)isacommonclinicalrefractorydiseasebe-
causeofitsunknownpathogenesisandetiology[ 2] .A
greatdealofexperimentprovesafactthatUCismainly
afectedbyinflammation, freeradicalsandlipidperox-
idationcausedbyit.Thus, itisexpectedtobeabated
byanti-inflammationandantioxidation[ 3-5] .Initialre-
searchofthisprojecthasprovedthatvolatileoilcan
significantlyimprovetheclinicalsymptomsofUCand
reducethecolonicmucosalpathologicallesionanddis-
easeactivityindex(DAI)score.Basedonthosedata,
thisresearchfocusesonantioxidativeandantinitrosati-
veefectsofvolatileoilfromA.longiligulareT.L.Wu
ondextransulfatesodium(DSS)-inducedulcerative
colitismiceusingbiochemicalmethodandimmunohis-
topathology.
1　Materials
1.1　Medicineandpreparation　AmomiSemenwas
colectedinWanning(HainanProvince, China)in
June, 2007 andidentifiedbyCHENGuo-biao, atradi-
tionalChinesedrugspecialistintheInstituteforDrug
ControlofHainanProvince, China.
Freshvolatileoilwasmadeintoemulsionwith
emulsifyingagentofgumArabic(contentofgumAra-
bic:3%).Weusedknifetoremovethecoatingofsul-
fasalazine, crusheditandpassedthrougha100 mesh
sieve.ItwasdissolvedingumArabicsolutiontomake
upthesuspension(contentofSASP:52 g/L;content
ofgumArabic:3%).Alabovewereintragastricaly
administeredwith0.2 mLper10 gbodyweight.The
suspensionandtheemulsionwerepreparedforevery
administration.
1.2　Mainreagent　dextransulfatesodium(Mr:
5000, FlukaLtd, USA);detectionkitsfornitricoxide
(NO), malondialdehyde(MDA), superoxidedismatase
(SOD)andtotalproteinquantificationkitbytheCoo-
massieBluemethod(JianchengBio-engineeringIn-
stitue.Nanjing.BatchNo:20070522);sulfasalazine
(SASP, 0.25 g×100s, ShanghaiSunweiPharmaceuti-
calCo., Ltd.Batchnumber:200710C20).
1.3　Experimentalanimals　SPFBalb/cmice(♂),
weighting20-24 g, werepurchasedfromtheCentralof
ExperimentalAnimalinGuangdongprovince.Certifi-
cateNo.:SCXK(Yue2003-0002).Oneweekbefore
theexperimentstarted, theywerehousedinanimalla-
boratoryoftheInstituteforDrugControlofHainan
Provinceinconditionsof22 ±2 ℃ and(55 ±15)%
RHona12-hrlight-darkcyclewithstandardfoodand
drink.
1.4　Maininstrument　Lowtemperaturecentrifuge
(3K15 , SigmaLtd, USA);UV-VisSpectrophotometer
(UV2450, SHIMADZULtd, Japan);parafinslicing
machine(CM1900 , LeicaLtd, Germany);Microscope＆
Medicine-PathologyAnalysisSystem (BX41, OLYM-
PUSLtd, Japan).
2　Methods
2.1　PreparationofvolatileoilfromA.longiligulare
T.L.Wu　Vapordistilationmethodwasadoptedto
extractthevolatileoil.FreshAmomiSemenwas
crushedwithshel, soakedfor1 h, distiledfor4 h,
saltedout, andplacedoveranightin4 ℃ refrigera-
tor.Inthesecondday, oillayerwascolected, de-
hydratedwithanhydroussodiumsulfatefor12 hand
filtrated.Accordingtodeterminationofvolatileoil
(appendixXD, ChP2005), thecontentofvolatileoil
was1.1mL/100 gseedweight.Thechemicalcompo-
sitionswereanalyzedbyGC.Thecontentofbornylac-
etatewas13% ofthevolatileoil.
2.2　DSS-inducedUCmodel　AccordingtoRefer-
ence[ 6] , experimentalulcerativecolitismodelswere
producedinmicebyprovidingthemwithdrinkingwa-
tercontaining4% DSSsolutionfor7 d.
2.3　Experimentalgroupingandadministration　60
Balb/cmalemice(SPF)wererandomlydividedinto6
groups, includingNormal, Model, HF-H, HF-M, HF-
L, SASP.Exceptnormalmiceweregivendistiledwa-
ter, othermiceweregivenfreedrinkingof4% dextran
sulfatesodium(DSS)solutionfor7 dtoinduceulcera-
tivecolitisdamage.VolatileoilandSASPweregiven
for3d2hafterthefifthadministrationofDSS.Normal
andModelmousereceivedonlythevehicle(3% gum
Arabicsolution)ascomparison.AccordingtoRefer-
ence[ 7] , LD50 ofvolatileoilfromA.longiligulareT.L.
Wuinmicewastestedtobe8.3458 mL/kgbybliss
method.ThedosageofHF-H, HF-MandHF-LGroup
was2 mL/kg, 1mL/kg, 0.5mL/kg, respectively.
2.4　MeasurementofNO, MDAcontentsandSODac-
tivityofcolonictissuebybiochemicalmethod　Thean-
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imalswerekiledonthe8thdaybycervicaldisloca-
tion.Thenitwaspaunchedandthewholecolonwas
takenout(fromileocecustoanus).Scisorspassed
verticalyalongthemesenteryandrinseditwith0 ℃
0.9% normalsaline.10%ofcolonicmucosahomoge-
nateswerepreparedwithfreezingsaline.Homogenates
weremicrocentrifugedat2500 rpmfor10 minat4 ℃
andthesupernatantwassavedformeasurementofNO,
MDAcontentsandSODactivity.Thedetermination
conditionsweretakenaccordingtotheinstructionsof
correspondingcommercialkits.Proteincontentwasde-
terminedusingtotalproteinquantificationkitbythe
CoomassieBluemethod.
2.5　MeasurementofiNOSexpressionincolonictis-
suebyimmunohistopathology　Thetissueswerefixed
in40 g/Lneutralybuferedformaldehyde, embedded
inparafin, serialysectionedat5 μm, andstainedby
SABC(StreptAvidin-BiotinComplex)method.Brief-
ly, thesectionsweredeparafinizedinxylene, rehydra-
tedingradedalcohols, washedindistiledwaterfor5
min, andincubatedin 0.3% hydrogen peroxide
(H2O2)inmethanoltoblockendogenousperoxidase
activityatroomtemperaturefor10 min.Thenthesec-
tionswerewashedin0.01 mol/L, pH7.4 phosphate-
buferedsaline(PBS)for10min, changedthree
times, andincubatedindilutednormalgoatserumto
diminishnon-specificbackgroundstainingat37℃ for
20 min.Theserumwasblotedawayfromthesections,
whichhadbeentreatedwiththeprimaryantiserum(1
∶100)at4 ℃ overnight.AfterbeingwashedinPBS,
thelinkingantibodieswereappliedandincubatedat37
℃ for20 min.ThentheABCmethodwasusedbyin-
cubatingthesectionsfor20 minafterbeingwashedin
PBS.Andthen, afteranotherwashing, thesections
weretreatedwith0.05% diaminobenzidine(DAB)in
0.1mol/L, pH7.6Tris-HClbufer, containing0.05%
H2O2 , for5-10 min.Afterbeingwashedindistiled
water, thesectionswerecounterstainedwithMayers
hematoxylin, dehydratedingradedalcohols, clearedin
xyleneandmountedinthepermount.Evaluativecrite-
ria:①PositiveiNOScelswerefoundincytoplasm;②
Positiveproductwasabrown-yelowgranule;③ Per-
centageofpositivecelswascalculatedonfivehigh-
foldvisualfield(200 fold)chosenfromeachsection,
and5 sectionswerechosenfromeachgroup.
2.6　Statisticalanalysis　Statisticalanalysiswasdone
withSPSSsystem(11.5).Theresultswereexpresed
asthex±s.DatawereanalyzedbyIndependentSample
ttest.AfterhomogeneitytestforvariancewithHomoge-
neityofVariances, LSDmethodwilbeoperatedinva-
riancehomogeneity;incontrast, TamhaneT2 method
wilbeoperatedinvariancenonhomogeneity.P<0.05
wastakenassignificant.P<0.01 wastakenashighly
significant.
3　Results
3.1　EfectsofvolatileoilfromA.longiligulareT.L.
WuoncontentsofMDA, NOandSODofcolonictisue
inmiceinducedbyDSS　Comparedwiththenormal
controlgroup, MDAcontentofcolonictissuewassig-
nificantlyincreasedinmodelmiceinducedbyDSS(P
<0.01), butSODlevelwassignificantlyreduced(P
<0.01).Itwassuggestedthatoxidativedamagein
UCmicewasinduced.Comparedwiththatofthemod-
elgroup, thecontentofMDAofcolonictisueofthe
micewassignificantlyreducedinHF-HgroupandHF-
Mgroup(P<0.01 orP<0.05), butSODlevelwas
significantlyincreased(P<0.01).Thesedatademon-
stratedthatvolatileoilfromA.longiligulareT.L.Wu
hadtheabilityofantioxidation.Therewasnosignifi-
cantdiferencebetweenvolatileoilfromA.longiligulare
T.L.Wuinlargeormediumdosetreatedgroupand
SASPgroup(P>0.05).
Comparedwiththatofthenormalcontrolgroup,
thecontentofNOofcolonictissuewassignificantlyin-
creasedinmodelmiceinducedbyDSS.Itissuggested
thatexcessiveNOparticipatedininflammationandtis-
suelesion.Comparedwiththatinthemodelgroup, NO
contentincolonictissueofthemicewassignificantly
reducedinHF-HgroupandHF-Mgroup(P<0.05 or
P<0.01), andthefunctionwasdose-dependent.
TherewasnosignificantdiferencebetweenHF-H
groupandSASPgroup(P>0.05).Thesedatademon-
stratedthatvolatileoilfromA.longiligulareT.L.Wu
hadtheabilitytoantagonizeNO, thediferenceofthe
efectoflargedosetreatedwasnotsignificantcompared
withthatofSASP.Tab.1showedthedetailedresults.
3.2　EfectsofvolatileoilfromA.longiligulareT.L.
WuoniNOSexpressionofcolonictisueinmicein-
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ducedbyDSS　Thecolonicmucosalepithelialcelcy-
toplasmofmiceinthenormalcontrolgroupwasstained
slightly.Fibercelsandvascularendothelialcelsin
thelaminabasialis, underthebasisandintheintersti-
tialofsurfaceepitheliumwerepositive, alofwhich
hadbrown-yelowgranulesincytoplasm.
Tab.1　Effectsofvolatileoilfrom A.longiligulareT.L.
WuoncontentsofMDA, NOandSODofcolonic
tissueinmiceinducedbyDSS(x±s, n=10)
Group MDA(nmol/mgprot)
NO
(μmol/gprot)
SOD
(U/gprot)
Normal 9.820±2.443 1.968±0.728 24.160±3.809
Model 30.679±8.667## 5.198±0.880## 9.763±1.002##
HF-H 12.798±3.334△△ 2.681±0.765△△ 20.677±3.153△△
HF-M 17.706±5.075△△ 3.672±0.908△ 17.841±3.663△△
HF-L 22.618±7.077 4.017±1.134 13.001±3.128
SASP 11.006±3.679△△ 2.119±0.973△△ 22.132±3.105△△
　　Note:#P<0.05, ##P<0.01vsNormalgroup;△P<0.05, △△P<
0.01 vsModelgroup
　　iNOSpositivecelsinthemodelgroupspread
throughoutthevisualfields, andincludedepithelial
celsofcolonicmucosaltisue, interstitialmacrophages
andvascularendothelialcels, alofwhichstained
brown-yelowincytoplasm.
TheexpresionofiNOSwaspositiveinalsurface
epithelialcelsandmostofepithelialcelsinglandular
cavity, butnegativeinlymphocyte.
Comparedwiththemodelgroup, volatileoilfrom
A.longiligulareT.L.Wuinlargeormediumdoseand
SASPcouldinhibitiNOSexpressionincolonicmucosal
tissue(P<0.01).Therewasnosignificantdiference
betweenHF-HgroupandSASPgroup(P>0.05).
ThesedatademonstratedthatiNOSexpressioncouldbe
significantlyreducedbyvolatileoilfromA.longiligulare
T.L.Wu, thediferenceoftheefectoflargedosewas
notsignificantcomparedwiththatofSASP.Theresults
ofiNOSexpresionwerepresentedinTab.2andFig.1.
4　Discussion
Accordingtorecentliteraturesathomeand
abroad, A.longiligulareT.L.Wucoordinatsperistalsis
ofstomachandintestines, improvesimmunologiccom-
petence, isanti-inflammatory, antioxidation, andan-
ti-plateletaggregation, inhibitsthrombosisandeases
pain.Therefore, itisworthofbeingdevelopedasa
cureforUC.Ulcerativecolitisisacryptogeneticin-
flammatorylesionwhichoccursincolonicmucosalay-
Tab.2　EffectsofvolatileoilfromA.longiligulareT.L.Wu
ontheexpressionofiNOSofcolonictissueinmice
inducedbyDSS(x±s, n=10)
Group n x±s Xmax Xmin RSD/%
Normal 10 3.70±0.95 5.00 2.00 25.64
Model 10 84.60±3.92## 90.00 80.00 4.64
HF-H 10 16.00±3.16△△ 21.00 11.00 19.76
HF-M 10 36.70±3.16△△ 43.00 33.00 8.62
HF-L 10 85.20±3.49 90.00 80.00 4.10
SASP 10 13.20±2.70△△ 17.00 10.00 20.45
　　Note:#P<0.05, ##P<0.01vsNormalgroup;△P<0.05, △△P<
0.01vsModelgroup
Fig.1　EffectsofvolatileoilfromA.longiligulare
T.L.WuontheexpressionofiNOSofco-
lonictissueinmiceinducedbyDSS(DAB
staining×200)
Note:A.Normal　 B.Model　 C.HF-H　 D.HF-M　 E.
HF-L　 F.SASP
er, withulcersmucosalerosionmainlyinvolvedmore
distalcolon, bloodymucus, abdominalpain, tenesmus
anddiarheaarethemainsymptoms.Thescreening
anddevelopmentofdrugsforanti-UCisstilinpro-
gressandthereismuchhopeforfindingitfromChi-
nesemedicinalplants.NOandoxygenfreeradicalplay
animportantroleinthepathogenesisofUC.Oxygen
freeradicalsgenerateagreatdealofMDAthroughlipid
peroxidationreactionandpromoteinflammatoryrespon-
sesasinflammatorymediators, whichcausesdamageto
tissues.ExcesiveNOgeneratedfromtheoxidativeme-
tabolismofL-argininebyiNOSwhichplaysaseriesof
complexbiologicalrolesinthepathogenicprocessesof
UC[ 7] .BytheinhibitionontheexpressionofiNOSand
deceasingthecontentofiNOS, theover-productionof
NOwasreduced, whichisonewaytoresearchandde-
velopenewdrugfortreatingUC[ 8] .
VolatileoilfromA.longiligulareT.L.Wuinlarge
ormediumdosecanreduceMDAlevelandincrease
SODactivitysignificantly.Theresultssuggestedthatit
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hastheabilityforantioxidation.Basedonthosedata
withbiochemicalmethodandimmunohistopathologyde-
tection, volatileoilfromA.longiligulareT.L.Wucan
inhibittheexpressionofiNOSanddecreasetheover-
productionofNO.
Therehasnotbeenthesystemticresearchofthe
efectofvolatileoilfromA.longiligulareT.L.Wuon
UC.Itisreportedforthefirsttimewhentheexpression
ofiNOSwasinhibitedbyvolatileoilfromA.longiligu-
lareT.L.Wu, theoverproductionofNOwasde-
creased, andtheinjuryofoxygenfreeradicalsandlip-
idperoxidationtocolonictissuewasaleviated, thein-
flammatoryinjuryofDSS-inducedmicewouldbere-
duced, whichcouldbetakenasoneofthemechanism
ofvolatileoilfromA.longiligulareT.L.Wufortreating
UC.Thisresearchcanprovideanin-depththeoretical
foundationforthepreventionandtreatmentofUCasa
basisforclinicalapplication.
PlentyofstudiesonchemicalconstituentsofA.
longiligulareT.L.Wuhavedemonstratedthatbornyl
acetate, limonene, camphene, camphor, p-cymeneand
othermaterailshadthefuctionofanti-inflammationand
antioxidation, whichexistinthevolatileoil.Therefore,
itisbelievedthatantioxidativeandantinitrosative
efectsofvolatileoilfromA.longiligulareT.L.Wuare
relatedtothesematerials.However, deep-goingand
concreteresearchesarestilrequired.
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氯化两面针碱对肝 、肾的毒性及酸性成纤维细胞生长因子对其的保护作
用研究
韦　敏 1 , 　刘丽敏 2 , 　李丹妮2 , 　刘华钢 2＊
(1.广西医科大学附属第五医院 ,广西 柳州 545005;2.广西医科大学 ,广西 南宁 530020)
收稿日期:2008-06-15
基金项目:国家自然科学基金项目(30850010),广西科学研究与技术开发计划项目(桂科改 0630002-E)
作者简介:韦　敏(1975-),女 ,硕士 ,副主任药师,主要从事临床药学及药物的合理应用方面的研究。 Tel:(0772)2663088
＊通讯作者:刘华钢(1956-),女 ,教授 ,博士生导师 ,主要从事中药新剂型 ,新制剂及作用机制的研究。E-mail:hgliu@163.com
关键词:氯化两面针碱;人胚肝细胞 L-02;人胚肾细胞 293;毒性;酸性成纤维细胞生长因子
摘要:目的:观察氯化两面针碱在体外对人胚肝细胞 L-02,人胚肾细胞 293的毒性作用 ,及酸性成纤维细胞生长因子(aF-
GF)对氯化两面针碱引起的肝 、肾细胞损伤的保护作用。方法:采用 MTT法检测不同浓度氯化两面针碱对人肝 、肾细胞
的毒性 , 及加入 aFGF后对肝 、肾细胞的 IC50值的影响。采用紫外分光光度法测定培养上清液中的 SOD、MDA、LDH值。
结果:aFGF可明显提高人胚肝细胞 L-02、人胚肾细胞 293的 IC50值。 aFGF保护组与氯化两面针碱损伤组的 SOD、MDA
和 LDH测定结果有显著性差异(P<0.05)。结论:氯化两面针碱对人胚肝细胞 L-02和人胚肾细胞 293有一定毒性 ,加
入 aFGF后 , 可明显减轻氯化两面针碱对人胚肝细胞 L-02和人胚肾细胞 293的毒性作用。
中图分类号:R285.6　　　　　文献标识码:A　　　　　文章编号:1001-1528(2009)09-1338-04
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第 31卷　第 9期
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