J Nat Med (2007) 61:131–137
DOI 10.1007/s11418-006-0100-0
ORIGINAL PAPER
Anticancer properties of panduratin A isolated from
Boesenbergia pandurata (Zingiberaceae)
Chandra Kirana Æ Graham Peter Jones Æ
Ian Roland Record Æ Graeme Howie McIntosh
Received: 10 April 2006 / Accepted: 8 August 2006 / Published online: 28 October 2006

The Japanese Society of Pharmacognosy and Springer 2006
Abstract Extract of Boesenbergia pandurata (Ka-
empferia pandurata) (Zingiberaceae) has been used as
a replacement for K. rotunda, the main ingredient of a
popular traditional tonic called ‘‘jamu’’ especially for
women in Indonesia. From our previous study, ethan-
olic extract of B. pandurata showed strong inhibitory
effects on the growth of cancer cells, similar to ethan-
olic extract of Curcuma longa. C. longa and its bioac-
tive compound, curcumin, have shown potential
anticancer activity in in vitro and in vivo studies and
have undergone clinical trials. Panduratin A, a chal-
cone derivative isolated from B. pandurata, was found
to inhibit the growth of MCF-7 human breast cancer
and HT-29 human colon adenocarcinoma cells with an
IC50 of 3.75 and 6.56 lg/ml, respectively. Panduratin A
arrested cancer cells labelled with Annexin-V and
propidium iodide in the G0/G1 phase and induced
apoptosis in a dose-dependent manner. In an animal
model study, male Sprague–Dawley rats were fed with
AIN diet containing ethanolic extracts prepared from
the equivalent of 4% by weight of dried rhizomes of B.
pandurata and C. longa. Aberrant crypt foci (ACFs)
C. Kirana (&)
I. R. Record
G. H. McIntosh
CSIRO Human Nutrition, P.O. Box 10041,
Adelaide BC, SA, Australia 5000
e-mail: chandra.kirana@csiro.au
C. Kirana
Department of Biology, Faculty of Mathematics
and Natural Sciences, Brawijaya University,
Malang, Indonesia
G. P. Jones
Faculty of Science, School of Agriculture,
Food and Wine, Adelaide University,
Adelaide, SA, Australia
were induced by two subcutaneous doses (15 mg/kg
body weight) of azoxymethane (AOM) 1 week apart.
The rats were killed 10 weeks later, and the ACFs
were assessed in the colon. At the dose given to rats, it
appeared that the extracts were not toxic. Total ACFs
were slightly reduced by B. pandurata extract com-
pared to control group but not significantly different.
Extract of B. pandurata may have a protective effect
against colon cancer but additional studies using dif-
ferent models, such as a breast cancer model, need to
be carried out.
Keywords Panduratin A
Boesenbergia pandurata

Zingiberaceae
Apoptosis
Cell cycle arrest

Azoxymethane
Aberrant crypt foci
Introduction
Medicinal herbs have always been used as traditional
primary health care agents, especially in Asian coun-
tries, and over the last 20 years, there have been rapid
changes in the popularity of the use of natural systems
to maintain health and for alternative therapy in Wes-
tern countries [1]. However, scientific studies on the use
of most traditional medicinal plants have not been
carried out to assure their efficacy and nontoxicity.
The plant Boesenbergia pandurata Schult (syn. Ka-
empferia pandurata Roxb.) (Zingiberaceae) is known
as ‘‘temu kunci’’ in Indonesia. The fresh rhizomes are
used in cooking and traditional medicine to treat
diarrhoea, dermatitis, dry cough, and mouth ulcers [2].
In times of shortage, B. pandurata has been used to
replace K. rotunda (‘‘kunci pepet’’, in Indonesian), the
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main ingredient in a popular traditional tonic espe-
cially for women, locally called ‘‘jamu’’. The effect of
the tonic has never been demonstrated clinically or in
animal experiments. Interestingly, an extract of B.
pandurata had a very strong growth-inhibitory activity
against human HT-29 colon adenocarcinoma and
MCF-7 breast cancer cells and was not toxic to the non-
transformed human skin fibroblast cells (SF3169),
while that of K. rotunda had no inhibitory activity [3].
This plant is also a popular condiment in Thailand.
Chemical studies of the rhizome of B. pandurata
have resulted in the isolation and identification of
several chalcones such as boesenbergin A, boesenber-
gin B, cardamonin, panduratin A, and dihydrometh-
oxychalcone, and flavanones such as pinocembrin,
pinostrobin, alpinetin and 5-hydroxy-7-methoxyflava-
none [4, 5]. The monoterpenoids geranial and neral, as
well as flavanones, have also been identified from the
rhizomes of B. pandurata [6].
Members of the Zingiberaceae family have been
reported to possess both antioxidant and anti-inflam-
matory activity. Such antioxidant and anti-inflamma-
tory compounds have often been shown to be effective
as anticancer agents [7]. In vitro studies on the extracts
of B. pandurata and their isolated compounds have
shown some beneficial pharmacological activities. For
example methanolic extracts of B. pandurata showed a
very strong inhibitory effect in the Epstein-Barr virus
(EBV)-activated test [8]. Cardamonin, pinocembrin,
panduratin A, and pinostrobin showed strong anti-
mutagen activity in the Ames test using Salmonella
typhimurium TA98 [9]. Tuchinda et al. [10] reported
that panduratin A had significant anti-inflammatory
activity in 12-O-tetradecanoylphorbol 13-acetate
(TPA)-induced ear edema in rats. Recently Yun et al.
[11] reported that panduratin A isolated from B.
pandurata inhibited the growth of HT-29 colon cancer
cells and induced apoptosis.
In this study, the anticancer properties of panduratin
A were evaluated using human HT-29 colon and MCF-
7 breast cancer cells, and the ethanolic extract of B.
pandurata was evaluated in the azoxymethane (AOM)-
induced aberrant crypt foci (ACF) model in rat. The
anticancer effects of the extract were compared with
the ethanolic extract of Curcuma longa (turmeric).
ACFs are microscopically identifiable precursor le-
sions of colon cancer found in rodents exposed to
certain procarcinogens but are also in human colonic
tissue and are considered to be a useful preneoplastic
marker of colon carcinogenesis [12]. The ACF model
study provides a rapid and reliable assay system and
has been used for the screening of potential chemo-
preventive agents [13, 14].
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J Nat Med (2007) 61:131–137
Materials and methods
Plant materials and chemicals
Roots and rhizomes of Boesenbergia pandurata Schl.
were purchased from the market place in Malang, East
Java, Indonesia and were characterised by Chandra
Kirana, MAgSc, PhD. A voucher of the specimen was
deposited at CSIRO Human Nutrition, Adelaide.
Samples were sliced, air-dried and brought to Adela-
ide, South Australia. Dried roots and rhizomes of C.
longa (turmeric) were purchased from Kriomill
(KrioKrush Basic Foods P/L, Singapore).
All chromatographic solvents were HPLC grade and
were purchased from BDH (Kilsyth, VIC, Australia).
Curcumin was purchased from Sigma Chemicals (St
Louis, MO).
Fractionation and preparation of panduratin A
Dried sliced roots and rhizomes (100 g) were homog-
enised and extracted with absolute ethanol (250 ml)
overnight at room temperature. The ethanol extract
was then vacuum filtered and the extraction repeated
three times. The combined ethanol extract was evap-
orated to dryness at 35C under vacuum and yielded
13.6% dry extract. The crude ethanol extract was
fractionated by preparative reversed-phase LC (Prep
Nova-Pak HR Prep LC column, particle size 6 lm,
200·25 mm; equipped with a guard column containing
the same material) using two different eluents; fraction
A was eluted with 1:1 methanol/water containing
0.025% v/v trifluoroacetic acid (TFA), and fraction B
was eluted with 100% methanol. The LC was run with
a flow rate of 20 ml/min.
Panduratin A was isolated from fraction B by pre-
parative reversed-phase LC using a mobile phase
consisting of a stepwise gradient of 60, 70, 75 and 80%
(v/v) aqueous methanol containing 0.025% (v/v) TFA.
Isolated panduratin A was then checked for its purity
by analytical HPLC (waters) using a modification of
the method by He et al. [16]. The HPLC system con-
sisted of a Licrosphere (Supelco, USA) RP C18 col-
umn (particle size 5 lm, 250·3.2 mm) equipped with a
guard column containing the same material. The
HPLC was run under gradient concentrations of 0.25%
acetic acid and 100% acetonitrile with a flow rate of
0.77 ml/min at 48C.
Panduratin A was characterised by nuclear magnetic
resonance (1HNMR) (600 MHz, Varian Inova) and
mass spectrometry LC ESI-MS (API-300, PE Sciex)
and identified by a comparison of the spectral data
[15].
J Nat Med (2007) 61:131–137
Cell lines and cell culture
HT-29 human colon adenocarcinoma cells and MCF-7
human breast cancer cells were purchased from the
American Type Culture Collection (ATCC) (Rock-
ville, MD). Tumour cell lines were maintained in
monolayer culture in Dulbecco minimum essential
medium (DMEM) supplemented with 10% heat-
inactivated foetal bovine serum (FBS), 20 mM HE-
PES (N-2-hydroxyethylpiperazine-N¢-2-ethanesulfonic
acid) buffer, 0.1% amphostat B and 5 lg/ml genta-
mycin in a humidified atmosphere of 5% CO2/95% air
at 37C.
DMEM, heat-inactivated FBS, HEPES, gentamycin,
amphostat B, PBS, and trypsin were all obtained from
Trace, Australia. MTT-tetrazolium salt [3-(4,5-dim-
ethylthiasol-2yl)-2,5-diphenyl tetrazolium bromide],
N,N-dimethyl formamide, and lauryl sufate (SDS)
were purchased from Sigma (St. Louis, MO).
Assessment of cell viability and proliferation
Exponentially growing cells were suspended at a den-
sity of 2–4·104 cells/ml in DMEM and treated with
panduratin A dissolved in dimethylsulphoxide
(DMSO) (final concentration of DMSO was 0.5%) and
with DMSO alone as the control in 96-well flat-bottom
plates for 24, 48 and 72 h. The viability of the cells was
assessed by MTT tetrazolium salt assay [17] using a
Spectra Max 250 (Microplate Spectrophotometer,
Molecular Devices, USA) at 570 nm. The IC50, i.e. the
concentration of the extract required to inhibit cell
growth by 50%, was determined.
Cell cycle analysis
About 200,000 cells/well were plated in six-well
plates overnight to allow cells to attach and were
treated with panduratin A dissolved in DMSO at
concentrations as above. After 24 h of treatment,
cells were harvested by using 0.01% trypsin/EDTA
and then resuspended in PBS containing 1% FBS.
The cells were fixed by dropwise addition of cold
70% ethanol while vortexing to avoid aggregation
and kept at –20C for at least 30 min. The cells were
then washed with PBS twice, suspended in 40 lg/ml
PI and 200 lg/ml RNAse (Sigma) in PBS and incu-
bated at room temperature for 30 min. Stained nuclei
were analysed for DNA-PI fluorescence using FAC-
Scan flow cytometry equipped with FACStation
running Cell Quest software (Becton Dickinson, San
Jose, CA).
133
Morphological examination of cancer cells
Cancer cells were grown on cover slips at a density of
100,000 cells/ml in six-well plates and allowed to attach
for 24 h and then treated with panduratin A dissolved
in DMSO. Five hundred microliters of cell suspension
from adhering and floating cells was obtained from the
wells, and slides were prepared using a cytocentrifuge
(Shandon Southern Products, Cheshire, UK). Slides
were air-dried, fixed in methanol and stained using
DiffQuick stain (Sigma, St. Louis, MO). One hundred
microliters of cell suspension on slides was stained with
1 mM Hoechst 33258 (Sigma). Chromatin condensa-
tion and nuclear fragmentation were observed with a
fluorescence microscope.
Apoptosis assays
About 200,000 cells/well were plated in six-well plates
overnight to allow cells to attach and were treated with
panduratin A dissolved in DMSO at concentrations of
3, 9, 18 and 26 lg/ml. After 48 h of treatment, both
adhering and floating cells were harvested and then
double-labelled with Annexin-V-Fluos (Roche) and
propidium iodide (PI) (Sigma) as described by the
manufacturer. Cells (10,000) were analysed using a
FACScan Flow Cytometry equipped with FACStation
running Cell Quest software (Becton Dickinson, San
Jose, CA), and total apoptotic cells were determined.
Animal study
Four week-old male outbred Sprague–Dawley rats
were purchased from the Animal Research Centre at
Murdoch University (Perth, Western Australia) and
separated randomly into control and treatment groups.
Animals were housed in wire cages to minimise co-
prophagy and maintained in an air-conditioned envi-
ronment of 23±2C with a 12:12 h light–dark cycle.
Rats were given free access to diet and water. All
experimental procedures involving animals were ap-
proved by the Commonwealth Scientific and Industrial
Research Organization (CSIRO) Health Sciences and
Nutrition Animal Experimentation Ethics Committee
and the University of Adelaide Animal Experimenta-
tion Ethics Committee before commencing the study.
Experimental design
Beginning at 5 weeks of age, rats were given different
experimental diets, which were based on AIN-93
specification [18]. There were three groups of 14 ani-
mals. Group 1 diet (control) contained semipurified
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AIN-93 only, the group 2 diet contained AIN-93 diet
mixed with an ethanol extract of B. pandurata and the
group 3 diet contained AIN-93 diet mixed with an
ethanol extract of C. longa. Extracts were prepared
from the equivalent of 4% by weight in diet of dried
rhizomes of B. pandurata and of turmeric. The dried
material (4%, i.e., 40 g dried rhizomes to make 1 kg
diet) was extracted with ethanol three times (material-
to-solvent ratio = 1:6) at room temperature. The eth-
anol extracts were combined and evaporated to reduce
the amount of ethanol. Extracts were then mixed with
the AIN-93 diet and dried at 35C in an oven over-
night. Diets were made fortnightly and kept in the
freezer until required. Diets were replaced every
3 days. At 7 weeks of age, rats received two subcuta-
neous injections of AOM 1 week apart at a dose rate of
15 mg/kg body weight. Rats were weighed weekly.
Rats were sacrificed using halothane/oxygen anesthesia
and exsanguinated via the abdominal aorta 10 weeks
after the second AOM injection. Colons were removed
for ACF counting.
ACF analysis
Colons were removed, flushed with buffer and opened
from caecum to anus and then fixed flat between two
pieces of filter paper in 10% buffered formaldehyde.
After a minimum of 24 h in formalin they were kept in
70% ethanol until ACFs were counted. Each colon was
placed for 7–10 min in a petri dish containing 0.2%
methylene blue dissolved in PBS. The colon was then
placed mucosa-side up on a microscope slide, and
ACFs were scored using a low power light microscope
(10·).
Statistical analysis
Data are reported as mean±SEM, and comparisons
were analysed by one-way analysis of variance
(ANOVA), with Bonferroni post-hoc test to identify
between-group differences (P<0.05) using Graphpad
Prism (version 2.0).
Results and discussion
Our previous in vitro study showed that an ethanolic
extract of B. pandurata had inhibitory activity on the
growth of cancer cells similar to that of C. longa. C.
longa is a member of Zingiberaceae that has been
extensively studied and shown to possess anticancer
activity [2]. An initial analysis of the bioactive com-
pounds in ethanol extracts of B. pandurata and C.
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J Nat Med (2007) 61:131–137
longa using the MTT tetrazolium salt assay revealed
that fraction B of B. pandurata was much more active
in inhibiting the growth of HT-29 colon cancer cells
than fraction A (Fig. 1). By comparison, fractions A
and B of C. longa both showed inhibitory activity, al-
though fraction A was more active than fraction B.
Curcuminoids (curcumin, demethoxycurcumin and
bisdemethoxycurcumin), the active compounds of C.
longa, were identified in fraction A by HPLC assay. A
chalcone derivative, panduratin A (2,6-dihydroxy-4-
methoxyphenyl)-[3¢-methyl-2¢-(3†-methylbut-2†-enyl)-
6¢-phenylcyclohex-3¢-enyl] methanone, was identified
in fraction B, isolated and characterised as described in
the methods. Panduratin A has the molecular formula
C26H30O4, which includes 12 aliphatic carbons (3CH3,
2CH2, 3CH, 2C=CH–), 12 aromatic carbons and one
methoxyl carbon [15]. The NMR data of panduratin A
were compared with and shown to be similar to pub-
lished data [9, 15].
The inhibitory activity of panduratin A was assessed
using HT-29 colon and MCF-7 breast cancer cells.
Figure 2 shows the viability of the cell lines treated
with panduratin A for 72 h at concentrations of 3, 9, 11,
and 18 lg/ml. It appeared that panduratin A was more
sensitive to MCF breast cancer than HT-29 colon
cancer cells. The IC50 of panduratin A in HT-29 cells
was 6.56 lg/ml and in MCF-7 cells was 3.75 lg/ml.
Panduratin A showed a cytostatic effect (100% inhi-
bition) on both HT-29 and MCF-7 cells at a concen-
tration of 9 lg/ml.
Cell-cycle analysis of HT-29 cancer cells treated
with panduratin A at 3, 9, 18 and 26 lg/ml for 24 h
showed alterations in the distribution of DNA content
Fig. 1 The growth inhibitory influence of fractions on HT-29
colon cancer cells at 72 h. Fraction A (A) was eluted with 1:1
methanol/water containing 0.025% v/v trifluoroacetic acid using
preparative reversed-phase LC, and Fraction B (B) was eluted
with 100% methanol of B. pandurata (BP) and C. longa (CL).
Viable cells were determined using MTT tetrazolium salt assay
as described under Materials and methods. Values are mean-
s±SE of three independent experiments
J Nat Med (2007) 61:131–137
Fig. 2 The viability and IC50 of MCF-7 and HT-29 cells after
72 h treatment at different concentrations of panduratin A.
Viable cells were determined by the MTT method. The results
are expressed as a percentage of the control (cells in 0.5%
DMSO). Values are means±SE of three independent experi-
ments
Fig. 3 HT-29 cancer cells in different phases of the cell cycle
after 24-h treatment with different concentrations of panduratin
A. The cells were fixed and stained with propidium iodide, and
the DNA content was analysed by FACScan flow cytometry.
Values are means±SE of three independent experiments
Fig. 4 Total apoptosis in HT-29 cancer cells after 48-h treatment
with different concentrations of panduratin A. The cells were
fixed and double-labelled with Annexin-V-Fluos and propidium
iodide and analysed by FACScan flow cytometry. Values are
means±SE of three independent experiments
135
(Figs. 3 and 4). There was an increase in the G0/G1
phase from 33% in untreated cells to 71% at 26 lg/ml.
The proportion of cells in the S phase was slightly re-
duced from 18.7% in untreated cells to 10.9% at 26 lg/
ml. By comparison, there was a decrease in the G2/M
phase from 36.8% in untreated cells to 15.4% at a
concentration of 26 lg/ml. Unlike panduratin A, which
arrested the cells in the G0/G1 phase, curcumin had a
blocking effect in the G2/M phase of the cell cycle in
many types of cancer cells [19].
HT-29 cells treated with panduratin A showed fea-
tures of apoptosis such as membrane blebbing, chro-
matin condensation and/or nuclear fragmentation and
apoptotic bodies when the cells were stained with
Hoechst 33258. Flow cytometry analysis using Annex-
in-V stain further revealed that panduratin A induced
apoptosis in HT-29 cells. At 48 h, 2.2% of cells treated
with 11 lg/ml of panduratin A underwent apoptosis
and the number of apoptotic cells increased to 16.7%
when treated with 26 lg/ml. Panduratin A induced
apoptosis by activation of caspase-3 associated with
PARP cleavage [11].
In a 13-week experiment, body weights of rats did
not differ among the dietary treatment groups over the
experiment period (Fig. 5). The final body weights
(means±SE) were as follows: 509±8 in control group,
513±11 in rats fed with the equivalent of 4% B.
pandurata and 519±8 in rats fed with the equivalent of
4% C. longa. In addition, the weight of spleens and
livers of rats did not differ among the groups (data not
shown), suggesting that the extracts at the concentra-
tions employed in this study were not toxic. Diet con-
taining 2% turmeric has been reported to inhibit
Fig. 5 Body weight (g) of rats fed with control AIN diet (AIN)
was not different from those fed with diet containing AIN mixed
with extract prepared from the equivalent of 4% by weight of
dried rhizomes of B. pandurata (BP) or C. longa (CL)
throughout 13 weeks of experiment (n=14)
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benzo[a]pyrene (BP)-induced forestomach tumours in
mice [20]. However, our previous study using a short-
term (6 weeks) AOM-induced colon cancer in rats
showed that diet containing 2% C. longa failed to af-
fect the formation of ACFs (data not shown). In this
study, diet containing extracts from the equivalent of
4% by weight of C. longa significantly reduced the
formation of total ACFs (P<0.01), with three to four
aberrant per foci (P<0.01). There was a reduction in
the formation of ACFs in rats fed with diet containing
4% by weight of B. pandurata, but it was not signifi-
cantly different compared to the control group (Fig. 6).
The antiproliferative activity of panduratin A, and
possibly other bioactive compounds in B. pandurata, to
block cells in the G0/G1 cell-cycle phase and to pre-
vent apoptosis may have benefits for reducing the
formation of ACFs in this in vivo study. In addition,
extracts of B. pandurata have also been shown to in-
duce mammalian phase-II chemoprotective and anti-
oxidant enzymes [21], and panduratin A has been
reported to have antimutagenic activity due to induc-
tion of quinone reductase (QR) [9]. Phase II enzymes,
such as gluthatione S-transferase (GST) and QR, are
important in cellular defence and metabolism, includ-
ing detoxification of electrophilic species and thereby
prevention of carcinogenesis [22]. In this respect,
panduratin A may offer similar protective effects.
Another anticancer activity of the extract that was
reported by Yun et al. [11] was that panduratin A
inhibited the expression of COX-2 in HT-29 cells. The
upregulation of COX-2 has been correlated with
pathological processes of inflammation and tumour
development [23].
Fig. 6 ACF formation in the colon of rats treated with different
diets: AIN-93 (AIN), AIN with added extract of Boesenbergia
pandurata (BP) and Curcuma longa (CL). Extracts of BP and
CL were prepared from 4% of dried material of B. pandurata
and C. longa respectively. Values are means±SD, n=14. Asterisk
indicates significant difference from control group of the same
column (P<0.01)
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J Nat Med (2007) 61:131–137
The results of this study show that panduratin A
isolated from B. pandurata has benefits as a chemo-
prevention agent to inhibit the proliferation of cancer
cells by blocking cells in G0/G1 phase and by inducing
apoptosis. The extract of B. pandurata reduced the
formation of ACFs in a colon cancer model study al-
though the difference was not significant. To the best of
our knowledge, this was the first animal study con-
ducted on B. pandurata. Further studies need to be
carried out to elucidate the anticancer activity of B.
pandurata. As panduratin A appeared to be more
sensitive toward MCF-7 breast cancer cells than HT-29
colon cancer, different animal models such as a breast
cancer study would be beneficial for improving the
understanding of the pharmacological actions of this
plant and its active compounds.
Acknowledgements The authors thank Dr Yoji Hayasaka of
the Australian Wine Research Institute for LC-MS data, Phil
Clements of the Department of Chemistry at the University of
Adelaide for NMR data and Dr Lindsay Dent of the Department
of Molecular Biosciences of the University of Adelaide for
permission to use the FACScan equipment. This project was
funded by AusAID and The Adelaide University and CSIRO
Collaborative Grant Program 2000.
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