全 文 ：相对的稳定, 使得细胞成为一种“永生化”状态, 因
此,端粒酶活性的增加与肿瘤的发生、发展密切相
关;临床资料表明造血系统的恶性肿瘤普遍表现出
端粒酶活性增强[ 8] ,其中以急性白血病端粒酶活性
最强, 在白血病的不同阶段其端粒酶水平也不完全
一样, 端粒酶活性的高低与白血病的进展程度相一
致,复发及难治性急性白血病的端粒酶水平明显高于
缓解及恶性程度较低的急性白血病, 端粒酶活性越高
的白血病患者其化疗效果及预后越差,存活率也越
低。因此,端粒酶活性的高低对于判断白血病的疗效、
恶性程度、预后及复发等均具有重要的临床意义。
端粒酶活性的变化与细胞凋亡的关系目前尚未
完全阐明。近期研究资料显示, 在细胞凋亡过程中,
端粒酶可能起重要的调节机制[ 9, 10] ,端粒酶活性下
降可以促进细胞的程序性死亡过程,端粒酶活性抑
制剂可以增加急性白血病细胞的凋亡率, 而且可以
增加其他化疗药物的临床疗效, “抗端粒酶疗法”有
可能成为一种广泛的白血病治疗方法,而且也是筛
选新型抗肿瘤药物的重要指标之一。本实验结果显
示,冬凌草甲素可显著降低 Raji 细胞的端粒酶活
性,抑制细胞的生长,诱导细胞发生凋亡, 这可能是
冬凌草甲素体外抗白血病作用的重要机制之一。
References:
[ 1]　Wu K M . Effect of oridonin on th e act ivity of tumor cel l
s odium pum p [J ] . C anc er Re s P rev Tr eat (肿瘤防治研究) ,
1994, 21( 4) : 208-209.
[ 2]　Yang S L, H an S Y, Zh ang Q, et al. S tu dy on th e ant imu-
t ion of oridonin [ J] . Carcinog T eratog Mutag (癌变·畸
变·突变) , 2001, 13( 1) : 8-10.
[ 3]　Yang S L, Zhang Q , Song A Y, et al . T he ef fect of or idonin
on UDS in th e primary cells of the lu ng and liver in rat [ J] .
H enan Med Univ (河南医科大学学报) , 2001, 36( 4) : 415-
418.
[ 4]　Wang J , Liu Q Y, Hu H Y, et al . Oridon in in duces apopto-
sis in human leukemia HL-60 cell s [ J ] . Chin Phar macol B ull
(中国药理学通报) , 2001, 17( 4) : 402-404.
[ 5]　Liu J J , Wu X Y, Pan X L, et al . Mechanism of oridonin in-
duced apop tos is on NB4 cells [ J] . Chin Tr adit Pat M ed (中
成药) , 2003, 25( 11) : 900-902.
[ 6]　Ikezoe T , Chen S S, Tong X J , et al. Oridon in ind uces
grow th inhib it ion and ap op tos is of a variety of human cancer
cel ls [ J] . Int J Oncol, 2003, 23( 4) : 1187-1193.
[ 7]　Han Q B, Li M L , L i S H, et al . Ent-kaurane diterpen oids
f rom Isod on rubescens var. lushanensi s [ J ] . Chem P harm
B ull , 2003, 51( 7) : 790-793.
[ 8]　Ohyash iki J H, Sashida G, Tauch i T. T elomeres and telom-
eras e in hematolog ic neoplas ia [ J] . Oncogene, 2002, 21( 4) :
680-687.
[ 9]　S aret zki G. T elomerase inhibit ion as cancer th erapy [ J] .
Cance r L ett , 2003, 194( 2) : 209-219.
[10]　Nakajima A, T auchi T, S ashida G. Telomeras e in hibit ion
enhances apoptos is in human acute leu kem ia cel ls : poss ibilit y
of ant it elomerase th erapy [ J ] . L eukemia, 2003, 17( 3) : 560-
567.
Effects of crocetin on experimental atherosclerosis in rats
DENG Yuan-x iong, QIAN Zhi-yu


, T ANG Fu-t ian
( Depar tment o f Pharmacolog y, China Pharmaceutical Univ ersity, Nanjing 210009, China )
　　Abstract: Object　T o study the ef fect o f crocet in ( CCT ) on experimental atherosclerot ic format ion in
rats. Methods　Ather osclerot ic r at models w ere replicated by administ ration of ex cessive v itamin D 2
( VD 2) fo llow ed by feeding a high-cholestero l diet . The blood samples w ere assayed fo r the content o f T C,
TG, LDL-C, HDL-C, MDA level, and the act ivity of SOD in serum . T he sect ions of aort ia and liv er were
examined. Results　High-and low -dosages o f CCT w ere found signif icantly to reduce serum T C, LDL-C,
and MDA level; and elevate serum HDL-C level , SOD act iv ity , and ant iatherosclerot ic index ( AAI) in
atherosclerot ic rats. T he histopatholog ical obser vat ion of aort ic arch show ed the allev iat ion o f atheroscle-
rot ic damage by CCT . Conclusion　CCT has obvious ant iatherosclerot ic ef fect in rats.
Key words : crocet in; ant iathero sclero sis; blood lipid; vitam in D2 ( VD2 )
西红花酸对大鼠实验性动脉粥样硬化的影响
邓远雄,钱之玉* ,唐富天
(中国药科大学 药理教研室,江苏 南京　210009)
摘　要: 目的　研究西红花酸对大鼠实验性动脉粥样硬化的影响。方法　采用给予大剂量维生素 D2( VD 2) 后饲喂
·777·中草药　Chinese T raditional and Herbal D rug s　第 35 卷第 7 期 2004年 7月

收稿日期: 2003-10-10作者简介:邓远雄( 1968—) ,男,湖南桂东人,主管药师,硕士研究生,主要从事生化药理研究。　E-m ail : dengyx1968@ tom. com
* 通讯作者　Tel: ( 025) 83271322
高胆固醇饲料诱发大鼠实验性动脉粥样硬化模型,测定大鼠血清总胆固醇 ( TC)、甘油三酯 ( TG )、低密度脂蛋白
( LDL-C)、高密度脂蛋白 ( HDL-C)、丙二醛 ( MDA ) 含量和超氧化物歧化酶 ( SOD) 活性。取主动脉和肝脏做病理
切片检查。结果　高、低剂量的西红花酸能显著降低动脉粥样硬化大鼠血清 T C、LDL-C 和 MDA 含量; 显著升高
血清 HDL-C 含量、SOD 活性和抗动脉粥样硬化指数 ( AAI )。病理切片结果表明, 西红花酸能明显减轻模型大鼠动
脉粥样硬化性损伤。结论　西红花酸具有显著的抗大鼠实验性动脉粥样硬化作用。
关键词: 西红花酸; 抗动脉粥样硬化; 血脂; 维生素 D 2
中图分类号: R286. 2　　　文献标识码: A　　　文章编号: 0253 2670( 2004) 07 0777 05
Introduction
　　Ather osclerosis, the principal cause of heart
at tack, st roke, and gangrene of the ext remit ies, is
responsible fo r 50% of all mortality o f them in the
USA, Europe, and Japan
[ 1]
. It is a disease o f the
arter ial injury characterized by the accumulat ion of
lipids, pro liferat ion of smooth muscle cells, and
calcificat ion
[ 2]
. T he animals such as r abbit , chick-
en, monkey , and pig can no t be w idely used as the
atherosclerot ic model because of v arious reasons.
It is w ell know n that the rat is not suscept ible to
atherosclerosis induced only by administ rat ion of
high cho lester ol diet ( HCD )
[ 1, 3]
, but administ ra-
tion of ex cessive vitam in D 2( V D2) and an ant ithy-
roid agent to rat in addition to high cholestero l diet
results in format ion o f atheromatous lesions
[ 4] .
Whether cr ocet in ( CCT ) , one of naturally occur -
ring components in Gard enia j asminoides Ell is [ 5] ,
w hich had hypolipidem ic effect [ 6] and ant iox idant
pr opert ies
[ 7- 10] , has ant iather osclerot ic ef fect on
this model has not been repor ted. Therefor e the
effect of CCT on athero scler osis using this model
w as studied.
1　Materials and methods
1. 1　Animals and reagents
Sprague-Daw ley r ats ( weighing 200—250 g,
purchased from A nimal Experiment Center of
China Pharmaceut ical University ) w ere housed in a
room [ ( 23±1) ℃ and ( 60±10) % humidity ]
under an art if icial 12-hour light / dark cycle ( 7: 00
a. m .—7: 00 p. m . ) .
The composit ion ( % ) of HCD: standar d chow
( 92. 6) , cho lestero l ( 2. 0) , lard ( 5. 0) , cholic acid
( 0. 2) , pr opy lthiouracil ( 0. 2) .
CCT , w ith purity of ov er 80% ( HPLC) , w as
ext racted fr om G. j asminoides and dissolved in
sodium carboxylmethylcellulose ( CMC-Na) ; VD2
was dissolved in the peanut oil; Simvastat in
( Sim ) , product of Hangzhou M er k Co. , L td. ,
w as formulated as w ater suspension.
1. 2　Experimental protocol
Experimental athero scler ot ic rat model w as
established according to the method of Mo risaki
[ 4]
w ith some modif icat ion. Af ter one w eek acclimat i-
zat ion, the rats w ere randomized into five groups
o f 10 animals each: no rmal g roup; model gr oup
( VD2+ HCD) ; CCT ( H) g roup ( VD2+ HCD+ 50
mg/ kg CCT ) ; CCT ( L) g roup ( VD 2+ HCD+ 25
mg/ kg CCT ) ; Sim gr oup ( VD 2+ HCD + 4 mg / kg
Sim ) . A ll rats ex cept for normal g roup w ere t reat-
ed by o ral administ rat ion of 300 000 IU / ( kg·d) of
VD 2 for three consecutive day s during w hich stan-
dard chow w as giv en. Meanwhile CCT or Sim w as
o rally g iv en to the corr esponding r ats. From the
fourth day , VD2-treated rats consumed HCD for 6-
w eek period in w hich CCT or Sim w as cont inuous-
ly adm inist rated. T he r ats w ere w eighed ever y tw o
days in order to adjust the do sage o f CCT o r Sim.
1. 3　Biochemical par ameters
　　Blood samples w ere collected from 12h-fast ing
animals by punctur e in the ret ro-o rbital sinus at
the end of the experiment . Serum T C, LDL-C,
HDL-C, t rigly ceride ( T G) w ere analy zed enzyma-
t ically using Kit f rom Beijing Zhongsheng Bio en-
g ineering Company . A nt i-atherosclerot ic index
( AAI ) w as calculated by the formula: AAI =
HDL-C/ ( TC - HDL-C ) . Serum SOD and MDA
were measur ed using Kit f rom Nanjing Jiancheng
Bioeng ineer ing Company. L iver was weighed and
l iv er index ( LI ) w as defined as liver weight ( g )
per 100 g body weight .
1. 4　Morpholo gical parameter
　　Animals were kil led at the end o f the experi-
ment , ao rtic arch and liver w ere f ixed in Bouins
·778· 中草药　Chinese T raditional and Herbal D rug s　第 35 卷第 7 期 2004年 7月
so lut ion, dehydrated, embedded in paraff in and
cut at 5 mm . The sect ions w ere stained w ith
hemalun-eo sin ( HE) .
In aorta, atherosclero sis w as scored as repo rt-
ed
[ 11]
. Focus w as g iv en to the main characteristics,
such as accumulat ion o f fo am cells in interlamellar
spaces, rect itude and fr agmentat ion of medial elas-
tic lamellae, abundance of collag en fibers, prolifer -
ated and disoriented smoo th muscle cells surr ound-
ing a l ipid-calcic cor e.
In liver, the severity o f damage w as def ined as
thr ee degrees o f heavy , moderate, and mild ac-
cor ding to lipid droplets and apopto tic changes.
1. 5　Statistical analysis
　　Data were expressed as x ±s and compared
w ith analysis of t-test .
2　Results
2. 1　Blood lipids and lipoproteins
As shown in T able 1, the ser um TC level in
model group w as about seven t imes that in no rmal
g roup, o f w hich LDL-C was 22-fold increased and
HDL-C decr eased by 40% . AAI w as surprising ly
low er and T G show ed no significant change indica-
t ing that athero scler osis model w as established su-
ccessfully . Compared w ith those in model group,
T C and LDL-C in CCT ( H) g roup w er e decreased
by 40% and 55%; LDL-C and AAI increased by
about 40% and 200%, respect ively; T G r emained
no significant change. T here w as no differ ence
betw een CCT ( H ) and CCT ( L) gr oups. In this
experiment, parameters in Sim g roup w ere similar
w ith those in CCT gr oups.
Table 1　Effect of CCT on blood lipids and lipoproteins in experimentally atherosclerotic rats ( x±s, n= 10)
Groups Dosage/ ( mg·kg- 1) T C/ ( mmol·L- 1) LDL-C / (mmol·L- 1) HDL-C/ ( mm ol·L- 1) T G/ (mmol·L- 1) AAI
Normal - 1. 77±0. 18 0. 43±0. 07 1. 01±0. 15 1. 72±0. 25 1. 38±0. 38
M odel - 12. 32±3. 16# # 9. 69±3. 85# # 0. 66±0. 21# # 1. 41±0. 43 0. 06±0. 03# #
CCT ( H) 50 7. 68±1. 89* * 4. 14±1. 90* * 1. 60±0. 23* * 1. 74±0. 68 0. 18±0. 07* *
CCT ( L) 25 7. 08±2. 59* * 4. 03±1. 73* * 1. 04±0. 27* * 1. 35±0. 81 0. 19±0. 07* *
S im 4 8. 18±2. 14* * 4. 69±1. 77* * 0. 95±0. 15* * 1. 41±0. 86 0. 15±0. 06* *
　　　# # P< 0. 01 v s normal group; * * P < 0. 01 vs model gr ou p
2. 2　Serum MDA and SOD
Rats in model g roup exhibited a higher con-
tent of MDA and a low er activity of SOD in serum
than tho se in normal g roup. In CCT group and Sim
gr oup, the MDA and SOD were improved, even
returned back to the no rmal level for CCT ( H )
gr oup and Sim g roup ( T able 2) .
Table 2　Effect of CCT on serum MDA and SOD in experi-
mentally atherosclerotic rats ( x±s, n= 10)
Groups　 Dosage/ ( mg·kg - 1) SO D/ (U·mL - 1) MDA/ (mmo l·L- 1)
Normal - 167. 49± 8. 16 5. 10±1. 33
Model - 158. 85±16. 22# 6. 83±1. 37#
CCT ( H) 50 169. 74±13. 09* 5. 15±1. 51*
CCT ( L) 25 166. 68±10. 60* 5. 37±1. 21*
Sim 4 168. 51±20. 00* 5. 35±1. 00*
　　　# P < 0. 05 v s normal group; * P < 0. 05 v s m odel group
2. 3　Morpho logical alterat ions in atherosclerot ic
rats
2. 3. 1　A ort ic lesions: Light micro scopy showed
no evident ao rtic lesions found in normal g roup
( F ig. 1-A ) . In CCT g roup, none o f the obvious
aort ic lesions could be seen as compared w ith the
model g roup, featuring more accumulation o f foam
cells in interlamellar spaces, rectitude and frag-
mentat ion of medial elast ic lamellae, abundance of
collag en f ibers, pro liferated and disoriented
smoo th muscle cells surrounding a lipid-calcic core
( F ig. 1-B ) . T he atherosclerosis w as sco re of
12. 0±2. 1 ( T able 3) , for model gr oup, and 4. 0±
0. 9 for CCT ( H ) g roup ( T able 3 ) . F ig. 1-C
show ed that no lipid deposit ion, foam cells,
w idening in int ima and no proliferat ion of smooth
muscle cel l, no increased ex t racellular matrix and
calcif icat ion in media. As w er e also in the Sim
g roup.
A-normal group　B-model gr ou p　C-CCT gr ou p
Fig. 1　Morphological structure of aorta
in atherosclerotic rats (×200)
2. 3. 2　Liver lesions and liver index : No abnor-
mal it ies were obser ved in the liver o f no rmal
·779·中草药　Chinese T raditional and Herbal D rug s　第 35 卷第 7 期 2004年 7月
gr oup. How ever, rat in model group demonst rated
the severe lipid droplets and apoptot ic changes
w hich w ere slight ly allev iated in the CCT and Sim
gr oup.
Table 3　Effect of CCT on pathological score of aorta
and liver index of experimentally
atherosclerotic rats ( x±s, n= 10)
Groups
Dosage
/ ( mg·k g- 1)
Liver index
/ ( g·100 g- 1)
Pathological score
of aor ta
Normal - 2. 7±1. 3 　　0
Model - 4. 7±0. 3# # 12. 0±2. 1# #
CCT (H ) 50 4. 4±0. 4* 4. 0±0. 9* *
CCT (L ) 25 4. 4±0. 5* 3. 8±0. 8* *
Sim 4 4. 6±0. 4 3. 3±0. 5* *
　　　# # P < 0. 01 v s normal group ; * P < 0. 05　 * * P < 0. 01 v s
model group
　　As shown in Table 3, the raised liver index
w as elevated markedly in model g roup in compari-
son w ith no rmal g roup. How ever, this parameter
w as significant ly reduced in CCT and Sim g roups.
3　Discussion
　　Administ rat ion of ex cessive VD 2 fo llow ed by
feeding HCD containing the ant ithyroid agent pro-
py lthiouracil caused severe hypercho lestero lem ia
and athero sclero tic lesions in rat [ 4, 11] , of w hich
pr opy lthiouracil w as r ecognized to pr oduce a mild
hypo thy roidism in o rder to provide a more favor -
able env ir onment fo r atherosclerisis development in
rats. The role VD 2 played seemed to be mediated
by the arterial calcification process in w hich my-
ocy tes serve as a local factor. It is induced by the
increase of conjunct iv e const ituents by calcifica-
tion, product ion of calcif iable substances ( glyco-
pro teins and glucoam inog lycans) , and modif icat ion
in their ow n environmental phy sico-chem ical condi-
tions favourable to calcium precipitat ion
[ 12]
.
In the present study, the morphological obser -
vat ion to aort ic arch by quant ify ing the histo-
patholog ial change completely confirmed the suc-
cessful establishment of the ather osclerot ic model
in r at . On this model, the ant iathero-sclerot ic ef-
fect o f CCT w as obser ved. M ain changes r epre-
sent ing the typical atherosclerosis, such as w iden-
ing , fo am cells format ion, lipid deposit ion in int i-
ma and calcificat ion, lipid depo sit io n, smoo th mus-
cle cell proliferat ion in media w er e rarely found in
CCT treated rat aorta compar ed w ith that in model
g roup. Also on this model, the damage of liver in
CCT groups w as also less serious than that of
model g roup in w hich severe lipid droplets and
apopto tic changes w ere char acterized. The smaller
l iv er index in CCT g roup could be also explained
by the fact that less lipid depo sited in the liver.
Biochemically , this combined treatment incr-
eased the serum T C level, of which most were
LDL-C w ith as much as 25 or 7 times that in the
control level, meanwhile, decreased the HDL-C
level significant ly. How ever , serum TG r emained
unchanged. This w as compatible to the repor t[ 3, 4] .
T he above finding s indicated that the fo rmat ion of
ather osclerot ic lesions in rats, w as mainly at-
t ributable to the high level o f TC instead o f TG.
Both high LDL-C and low HDL-C level favo red the
ather osclerosis because of the poo r AAI. Such dis-
or ders w ere implied in the athero genesis
[ 1]
by accu-
mulat ion o f macr ophages lo aded w ith lipid ( foam
cell) deriv ed f rom monocy tes. CCT at both high
and low doses, enjoyed its po tentially ant i-
ather osclerot ic ef fect part ly by significant ly low er-
ing serum T C and LDL-C, especially by elevat ing
HDL-C which protects against the pro gression of
ather osclerosis no t only by t ranspor ting the choles-
terol from foam cells in the arterial wall to the liv-
er, but also by pro tect ing the endothel ium from in-
jury[ 13] result ing in prevent ion of leukocyte and
platelet adhesion and in maintenance of the ant ico-
agulant propert ies o f endothelium, and by inhibi-
t ion o f smooth muscle cell pro liferation. T hese ef-
fects of CCT w ere similar to that of Sim, a HMG-
CoA inhibitor .
Ox idat iv e st ress, specif ically the oxidat ion of
LDL, has long been suspected of hav ing a crit ical
r ole in the development of ather osclerosis, and an-
t iox idants have been expected to have potent ial as
ant iatherogenic agents. As an antiox idant , CCT s
mechanism of ant io xidat ion could part ly explain it s
ant iatherosclerot ic ef fect by raising serum SOD and
low ering serum MDA. How ever , the o ther mecha-
nism of CCT s ef fect on antiathero scler osis is being
further studied in our labo rato ry.
·780· 中草药　Chinese T raditional and Herbal D rug s　第 35 卷第 7 期 2004年 7月
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麻黄汤及单味麻黄中麻黄碱与伪麻黄碱在小鼠组织中的药动学研究
魏凤环, 罗佳波
,沈　群,陈飞龙
(第一军医大学 中药药剂重点实验室,广东 广州　510515)
摘　要: 目的　分析麻黄汤 ( HED) 和单味麻黄 ( HE) 中麻黄碱 ( ephedr ine, E)、伪麻黄碱 ( pseudoephedr ine, PE)
在小鼠脑、肺、心、肝、肾的动态变化, 探讨 HED 配伍的意义。方法　用 GC -MS/ SIM 法, HP-5 弹性石英毛细管
( 25 m×0. 2 mm) ,载气 He,无分流进样, 柱初温 120 ℃, 1 min 后以 10 ℃/ min 升至 185 ℃, 再以 30 ℃/ min 升至
245 ℃,保持 5 min, 选择离子 ( SIM , m/ z = 154, 265) ,进样量 1
L。结果　建立了组织中 E、PE 的测定方法。HED
及 HE 中 E、PE 在各组织中的动力学变化不一致,且 HED、HE 中 E 或 PE 在同一组织中的动力学参数亦不同。其
中 E 在脑、肺、肾的分布量是 HE> HED。结论　本法稳定、可靠,适于 E、PE 在组织中的含量测定。HED 中桂枝、
杏仁、甘草影响了 E、PE 在小鼠组织的动力学过程。
关键词: 麻黄碱; 伪麻黄碱; 配伍; GC-MS/ SIM ; 药动学
中图分类号: R285. 61　　　文献标识码: A　　　文章编号: 0253 2670( 2004) 07 0781 04
Pharmacokinetics of ephedrine and pseudoephedrine from Herba Ephedrae
Decoction and Herba Ephedrae in mice tissues
WEI Feng-huan, LUO Jia-bo, SHEN Qun, CHEN Fei-long
( Key Labo ra tor y o f Pharmaceut ical Reasearch of T raditional Chinese Medicine,
F ir st M ilitar y Medica l Univ ersity, Guangzhou 510515, China)
Abstract: Object　T o analy ze the pharmacokinet ics change of ephedrine ( E) and pseudoephedrine
( PE ) in H erba Ep hed rae Decoction ( HED) and H er ba Ephedrae ( HE ) in the br ain, lung , hear t , liver,
and kidney o f mice to discuss the meaning of compatibility of the prescr ipt ion. Methods　Gas chromato g-
raphy-mass spect rometry w ith selected ion monitoring ( GC-M S/ SIM ) was used. GC-M S condit ions w ere:
capillary co lumn HP-5 ( 25 m×0. 2 mm ) , Hel ium as car rier gas, non-split inject ion, column temperature
120 ℃ ( 1 min) 10 ℃/ min 185 ℃ 30 ℃/m in 245 ℃ ( 5 m in) , w ith 1. 0 mL/ min runof f , SIM (m/ z = 154,
·781·中草药　Chinese T raditional and Herbal D rug s　第 35 卷第 7 期 2004年 7月

收稿日期: 2003-10-15基金项目:国家自然科学基金重点资助项目 ( No 30030150)作者简介:魏凤环( 1976—) ,女,山东省人,博士研究生,研究方向为方剂配伍规律及中药新药的研究开发。
* 通讯作者　Tel: ( 020) 61648266　E-m ail : ljb@ fimmu. com