Flavonoid glycosides from microtea debilis and their cytotoxic and anti-inflammatory effects

Article abstract of DOI:10.1016/j.fitote.2010.08.014

Two new 5-O-glucosylflavones, 5-O-β-D-glucopyranosyl cirsimaritin (1) and 5, 4'-O-β-Ddiglucopyranosyl cirsimaritin (2), four known flavonoids, cirsimarin (3), cirsimaritin (4), salvigenin (5), 4', 5-dihydroxy-7- methoxyflavone (6), and a norisoprenoid, vo

Full text of DOI:10.1016/j.fitote.2010.08.014

Fitoterapia 82 (2011) 168–172
Contents lists available at ScienceDirect
Fitoterapia
journal homepage: www.elsevier.com/locate/fitote
Flavonoid glycosides from Microtea debilis and their cytotoxic and
anti-inflammatory effects
b
c
d
c
Naisheng Bai a, Kan He a, , Marc Roller , Ching-Shu Lai , Xi Shao , Min-Hsiung Pan ,
⁎
Antoine Bily a, Chi-Tang Ho d
a
Naturex, Inc., 375 Huyler St., South Hackensack, NJ 07606, United States
Naturex SA, Site d'Agroparc BP 1218, 84911 Avignon Cedex 9, France
Department of Seafood Science, National Kaohsiung Marine University, No.142, Haijhuan Rd., Kaohsiung 81143, Taiwan
Department of Food Science, Rutgers University, 65 Dudley Road, New Brunswick, NJ 08901, United States
b
c
d
a r t i c l e i n f o
a b s t r a c t
Article history:
Received 15 July 2010
Accepted in revised form 20 August 2010
Available online 8 September 2010
Two new 5-O-glucosylflavones, 5-O-β-D-glucopyranosyl cirsimaritin (1) and 5, 4′-O-β-D-
diglucopyranosyl cirsimaritin (2), four known flavonoids, cirsimarin (3), cirsimaritin (4),
salvigenin (5), 4′, 5-dihydroxy-7-methoxyflavone (6), and a norisoprenoid, vomifoliol (7),
have been isolated from the aerial parts of Microtea debilis. All isolates were tested for
cytotoxicity in human cancer cell lines (Hep G2, COLO 205, and HL-60) and anti-inflammatory
activities in LPS-treated RAW264.7 macrophages. Compound 6 was found to be a potent
inhibitor to nitrite production in macrophages. Compounds 2, 4, 6, and 7 showed moderate
anti-proliferative activity against COLO-205 cells with IC50 values of 7.1, 13.1, 6.1, and 6.8 μM,
respectively.
Keywords:
Microtea debilis
5-O-β-D-Glucopyranosyl cirsimaritin
5, 4′-O-β-D-Diglucopyranosyl cirsimaritin
Human cancer cell lines (Hep G2, COLO 205,
HL-60)
© 2010 Elsevier B.V. All rights reserved.
Anti-inflammatory
1. Introduction
ethanol extract of the aerial parts of M. debilis was subjected
to column chromatography over SP 70, MCI GEL CHP-20P,
Microtea debilis Sw. (Phytolaccaceae), commonly known as
weak jumby pepper, is a small creeping annual weed originating
from South America. It is used in folk medicine to treat cough,
stomach ache [1], acute renal failure, and proteinuria [2,3]. It has
been reported that the anti-proteinuric effect of the plant is
probably related to the adenosine-A1 antagonistic action of
cirsimarin, one of the major flavonoids found in M. debilis [2,3].
Cirsimarin was also found to exert a strong lipolytic activity
with 20 times more potency than caffeine to trigger
lipid mobilization [4]. In vitro, cirsimarin induced a dose-
dependent inhibition of lipid peroxidation, indicating moderate
antioxidant activity, and exerted a direct action on hydrogen
peroxide production by adipose tissue cells [5].
and Sephadex LH-20 resins to afford a total of seven
pure compounds. Two of the isolates were unusual flavone
glycosides possessing an O-β-D-glucopyranosyl functionality at
the C-5 position, 5-O-β-D-glucopyranosyl cirsimaritin (1) and
5, 4′-O-β-D-diglucopyranosyl cirsimaritin (2). Five known
compounds were identified as cirsimarin (3) [3], cirsimaritin
(4) [3], salvigenin (5) [6,7], 4′, 5-dihydroxy-7-methoxyflavone
(6) [8], and vomifoliol (7) [9,10] by comparison of the observed
spectroscopic data with those of the literature. Compounds 5–7
were isolated from this plant for the first time.
2. Experimental
As a part of our continued effort to find phytochemicals with
antitumor and anti-inflammatory activities from herbs, a 95%
2.1. General
Optical rotations were measured with a Perkin-Elmer 241
polarimeter. FT-IR was performed on a Perkin-Elmer BX
system (Perkin-Elmer Instruments, Norwalk, CT) with a
⁎
Corresponding author. Tel.: +1 201 440 5000; fax: +1 201 342 8000.
E-mail address: k.he@naturex.com (K. He).
0367-326X/$ – see front matter © 2010 Elsevier B.V. All rights reserved.
doi:10.1016/j.fitote.2010.08.014

N. Bai et al. / Fitoterapia 82 (2011) 168–172
169
OR'
MIRacle ATR accessory (Pike Technologies, Madison, WI). UV
spectra were acquired on a Shimadzu, UV-1700 UV–Visible
Spectrophotometer. The 1H and 13C NMR spectra were
recorded on an Inova-400 (1H at 400 MHz) instrument
(Varian Inc., Palo Alto, CA) with DMSO-d6 as the solvent
(Aldrich Chemical Co., Allentown, PA). The 2D correlation
spectra were obtained using standard gradient pulse
sequences of Varian VNMR software and performed on 4-
nuclei PFG AutoSwitchable or PFG Indirect Detection probes.
HRESIMS was run on a Waters Micromass LCT (Waters
Corporation, Milford, MA) or a Thermo Scientific LTQ Orbitrap
mass spectrometers (Thermo-Finnigan, San Jose, CA). GC–MS
analysis was carried out on an Agilent HP 6890 Series
Gas Chromatograph system and Agilent HP 5973 Mass
Spectrometer (Santa Clara, CA) with Rxi-1ms capillary GC
column (60 m×0.25 mm ID×1.0 μm). HPLC analysis was
performed on an Agilent 1100 LC series and the column used
was 250×4.6 mm i.d., 5 μm, Luna C-8 (Phenomenx Inc.) with
a flow rate of 1.0 mL/min. The solvent system consisted of a
linear gradient that started with 5% (v/v) MeCN in 0.1% TFA/
H2O, increased to 95% MeCN over 40 min, and increased to
100% MeCN within 5 min. At the end of the run, 100% MeCN
was allowed to flush the column for 5 min and an additional
10 min of post run time was set to allow for equilibration of
the column. The UV detector was set at 280 nm wavelength
and column temperature was ambient.
4'
8
O
O
CH3O
CH3O
1'
5
OR
Fig. 1. Structures of 1–4 from Microtea debilis. 1 R=β-D-glucopyranosyl, R′ =H.
2 R=R′=β-D-glucopyranosyl. 3 R=H, R′=β-D-glucopyranosyl. 4 R=R′=H.
2016, 1638, 1605, 1514, 1453, 1355, 1253, 1049, 1010, and
832 cm−1 1H and 13C NMR data, see Table 1; HRESIMS: m/z
;
477.1415 [M+H]+ (calcd for C23H25O11, 477.1397).
Compound (2, Fig. 1), 5, 4′-O-β-D-diglucopyranosyl
cirsimaritin, yellow amorphous powder, [α]2D5 −1.2 (c 0.25,
DMSO); UV (MeOH) 218, 268, and 325 nm; IR νmax 3358,
2363, 2020, 1637, 1605, 1514, 1455, 1355, 1253, 1116, 1010,
and 833 cm−1 1H and 13C NMR data, see Table 1; HRESIMS:
;
2.2. Plant material
m/z 639.1929 [M+H]+ (calcd for C29H35O16, 639.1925).
The aerial parts of M. debilis were collected in Surinam.
The plant was identified by macroscopic examination, TLC,
and HPLC methods compared with authentic sample.
A voucher specimen (MT105003) was deposited in the
Herbarium of Naturex, Inc. (South Hackensack, NJ).
2.4. Aglycone analysis
A total of 10 mgof 1 was dissolved in 1 mL of H2O along with
0.1 mL of conc. HCl. The solution was heated at 65 °C for 2 h and
dried under vacuum. The residue was washed with H2O three
times to remove sugar and the aglycone (4) was obtained
for NMR analysis. 1H NMR (400 MHz, DMSO-d6): δ 6.83 (1H, s,
H-3), 6.91 (1H, s, H-8), 7.95 (2H, d, J=6.0 Hz, H-2′, 6′), 6.92
(2H, d, J=6.0 Hz, H-3′, 5′), 3.72 (3H, s, 6-OCH3), 3.90 (3H, s, 7-
OCH3). 13C NMR (100 MHz, DMSO-d6): δ 164.1 (C-2), 102.7 (C-
3), 182.3 (C-4), 152.1 (C-5), 131.9 (C-6), 158.7 (C-7), 91.6 (C-8),
152.7 (C-9), 105.1 (C-10), 121.1 (C-1′), 128.6 (C-2′ and 6′),
116.0 (C-3′ and 5′), 161.4 (C-4′), 56.5 (7-OCH3), 60.1 (6-OCH3).
ESIMS: m/z 315 [M+H]+, C17H15O6.
2.3. Extraction and isolation
The air-dried and powdered aerial parts (420 g) were
extracted with 95% EtOH three times at 50 °C. The
combined EtOH extracts were concentrated (61 g) and was
chromatographed on SP 70 resin (Sigma Chemical Co., St. Louis,
MO) (1.0 L, 5.5 cm×75 cm), eluted with gradient H2O–EtOH
system (1:0, 10:1, 5:1, 3:1, 2:1, 1:1, 1:2, and 0:1). In each
gradient step, 2.5 L of eluent was used and 0.5 L was collected as
one fraction. A total of 40 fractions were collected in which
fractions with similar HPLC chromatograms were combined and
concentrated. Fractions10–11 were chromatographed over MCI
GEL CHP-20P (Mitsubishi Kasei Co.) (100 mL, 2.5 cm×40 cm)
and eluted with gradient H2O–MeOH (9:1→0:1). The fractions
collected from CHP-20P were further purified on Sephadex LH-
20 (Sigma Chemical Co.) (100 mL, 2.5 cm×40 cm) resulted in
the isolation of 1 (31 mg, tR=10.0 min). In the same manner,
repeated chromatography of different fractions using MCI GEL
CHP-20P and Sephadex LH-20 yielded 2 (5 mg, tR=8.1 min,
fractions 7–8), 3 (120 mg, tR=12.7 min, fractions 12–15), 4
(65 mg, tR=27.4 min, fractions 21–36), 5 (3 mg, tR=27.8 min,
fraction 37), 6 (4 mg, tR=29.2 min, fractions 39–40), and 7
(4 mg, tR=9.9 min, fractions 7–8).
2.5. Sugar analysis
A solution of 1 or 2 (2.0 mg each) in 1 N HCl (1 mL) was
stirred at 85 °C for 3 h. The solution was evaporated under a
stream of N2. The residue was dissolved in 0.1 mL of Tri–Sil Z (N-
trimethylsilylimidazole: pyridine: 1:4, Pierce Biotechnology,
Rockford, IL) and the mixture was allowed to react at 60 °C for
15 min. After drying under a stream of N2, the residue was
dissolved in 1 mL of water and partitioned with 1 mL of CH2Cl2.
The CH2Cl2 layer was analyzed by GC–MS (Rxi-1ms GC column,
temperatures for inlet injection 200 °C; temperature gradient
system was used for the oven, starting at 120 °C for 1 min and
then raised to 280 °C at rate of 40 °C/min). D-Glucose was
identified for 1 and 2 by comparison with retention time of
authentic D-glucose (tR=9.89 min) after treatment in the same
manner with Tri–Sil Z.
Compound (1, Fig. 1), 5-O-β-D-glucopyranosyl cirsimaritin,
yellow amorphous powder, [α]2D5 −69.9 (c 0.76, DMSO); UV
(MeOH) 217, 235, 266, and 330 nm; IR νmax 3310, 3194, 2164,

170
N. Bai et al. / Fitoterapia 82 (2011) 168–172
Table 1
NMR data of 1 and 2 (DMSO-d6).
pos.
1
2
HMBC b
δΗ (J in Hz)
δC mult.
HMBC
a
δΗ (J in Hz)
δC mult.
2
3
161.6, qC
105.5CH
160.8 qC
106.3 CH
6.74 s
7.26 s
2,4,10,1′
NOE: 2′,6′
6.85 s
2,4,10,1′
NOE: 2′,6′
4
5
6
7
8
9
177.5 qC
148.2 qC
139.9 qC
158.2 qC
97.8 CH
154.0 qC
110.8 qC
61.0 CH3
56.7 CH3
121.1 qC
128.3 CH
116.1 CH
161.1 qC
116.1 CH
128.3 CH
105.4 CH
74.1 CH
77.8 CH
69.9 CH
76.6 CH
60.8 CH2
177.4 qC
148.0 qC
139.8 qC
158.2 qC
97.8 CH
153.9 qC
110.8 qC
60.8 CH3
56.6 CH3
123.7 qC
127.9 CH
116.5 CH
160.1 qC
116.5 CH
127.9 CH
105.2 CH
74.0 CH
77.7 CH
69.8 CH
76.6 CH
60.6 CH2
4,6,7,9,10
7.33 s
4,6,7,9,10
10
6-OCH3
7-OCH3
1′
2′
3′
4′
5′
6′
1″
2″
3″
4″
5″
6″
3.79 s
3.95 s
6
3.79 s
3.97 s
6
7; NOE: 8
7, NOE: 8
7.94 dd (6.8,1.6)
6.92 dd (6.8,1.6)
2,4′,6′
1′,4′,5′
8.06 d (8.8)
7.19 d (8.8)
2,4′,6′
1′,4′,5′
6.92 dd (6.8,1.6)
7.94 dd (6.8,1.6)
4.77 d (7.6)
3.34 m
3.14 m
3.23 m
3.22 m
3.69 d (11.6)
3.34 m
1′,3′,4′
2,2′,4′
5
7.19 d (8.8)
8.06 d (8.8)
4.79 d (8.0)
3.38 m
3.13 m
3.25 m
3.45 m
3.71 m
3.65 m
1′,3′,4′
2,2′,4′
5
1″, 3″
1‴
2‴
3‴
4‴
5‴
6‴
5.03 d (7.6)
3.33 m
3.17 m
3.20 m
3.48 m
99.8 CH
73.2 CH
77.2 CH
69.6 CH
76.5 CH
60.6 CH2
4′, NOE: 3′,5′
3.67 m
a
Carbon multiplicities were determined by DEPT experiments.
Two and three bonds H–C correlations.
b
2.6. Cytotoxic analysis
scanning with an enzyme-linked immunosorbent assay reader
with a 570 nm filter.
The COLO-205 cell line was isolated from human colon
adenocarcinoma (ATCC CCL-222); human promyelocytic
leukemia (HL-60) cells were obtained from American Type
Culture Collection (Rockville, MD). The human Hep G2
hepatocellular carcinoma cells (BCRC 60025) were obtained
from the Food Industry Research and Development Institute
(Hsinchu, Taiwan). COLO-205 and HL-60 cell lines were
grown at 37 °C in 5% CO2 atmosphere in RPMI. Hep G2 cells
were grown in Dulbecco's minimal essential medium
(DMEM) supplemented with 10% heat-inactivated fetal calf
serum (Gibco BRL, Grand Island, NY), 100 units/mL of
penicillin and 100 μg/mL of streptomycin, and kept at 37 °C
in a humidified atmosphere of 5% CO2 in air. Selected
compounds were dissolved in dimethyl sulfoxide (DMSO).
Propidium iodide was obtained from Sigma Chemical Co. (St.
Louis, MO).
2.7. Nitrite assay
The RAW264.7 cells were treated with isolated compounds
and LPS (Escherichia coli O127:E8, molecular weight, 60 kDa,
Sigma Chemical Co.) together or LPS alone. The supernatants
are harvested and the amount of nitrite, an indicator of NO
synthesis, is measured by use of the Griess reaction. Briefly,
supernatants (100 μL) are mixed with the same volume of
Griess reagent (1% sulphanilamide in 5% phosphoric acid and
0.1% naphthylethylenediamine dihydrochloride in water) in
duplicate on 96-well plates. After incubation at room
temperature for 10 min, absorbance at 570 nm is measured
with an ELISA reader (Thermo Labsystems Multiskan Ascent,
Finland).
Cell viability was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2,
5-diphenyltetrazolium bromide (MTT) assay [11]. Briefly, human
cancer cells were plated at a density of 1×105 cells/mL into 24
well plates. After overnight growth, cells were pretreated with
series of concentration of test compounds for 24 h. The final
concentration of DMSO in the culture medium was b0.05%. At the
end of treatment, 30 μL of MTT was added, and the cells were
incubated for a further 4 h. Cell viability was determined by
3. Results and discussion
Compound 1 was obtained as a light yellow amorphous
powder. The HRESIMS displayed a protonated molecular ion
at m/z 477.1415 [M+H]+, suggesting a molecular formula of
C23H24O11. The IR spectrum of 1 showed absorptions
indicative of a hydroxyl group at 3310 cm−1 and an aromatic
ring at 1638 and 1605 cm−1. Its UV spectrum showed

N. Bai et al. / Fitoterapia 82 (2011) 168–172
171
Table 2
Effect of 1–7 on LPS-induced nitrite production in RAW 264.7 macrophages.
Table 3
Effect of 1–7 on the growth of various human cancer cells.
Compound
HL-60
Cell line
Hep G2
COLO 205
1
2
3
4
Control
LPS
20 μg/mL
40 μg/mL
1.0 0.1
1.0 0.1
1.0 0.1
1.0 0.1
IC50 (μM)
37.6 1.5
30.1 1.1
31.0 2.4
37.6 1.5
24.9 1.9
25.2 1.5
37.6 1.5
28.8 1.3
27.2 1.5
37.6 1.5
20.1 1.5
12.2 2.1
1
2
3
N100
N100
N100
N100
50.4 2.9
N100
N100
7.1 1.0
N100
4
5
61.0 2.2
N100
N100
N100
13.1 0.6
N100
5
6
7
Control
LPS
20 μg/mL
40 μg/mL
1.0 0.1
37.6 1.5
28.0 0.8
24.0 0.9
1.0 0.1
37.6 1.5
2.1 0.9
0.0 0.2
1.0 0.1
37.6 1.5
25.5 1.4
18.4 2.9
6
7
55.9 3.1
55.6 0.5
5.0 0.6
50.0 4.8
45.5 2.0
10.0 4.3
6.1 0.3
6.8 0.5
11.9 4.9
Doxorubicin a
Each experiment was independently performed three times and expressed
as mean SE.
a
Positive control.
maximum absorptions at 217, 235, 266, and 330 nm, typical
of a flavone. The 13C NMR spectral signals revealed the
presence of a flavonoid with two methoxy groups (δ 56.7,
61.0) and one glucopyranosyl unit (δ 105.4, 74.1, 77.8, 69.9,
76.6, and 60.8). The 1H NMR spectrum of 1 contained signals
of a 4′-hydroxy substituted B-ring with an AB spin system at δ
7.94 (2H, dd, J=6.8, 1.6 Hz, H-2′, 6′) and 6.92 (2H, dd, J=6.8,
1.6 Hz, H-3′, 5′). The presence of a singlet at δ 7.26
was attributed to the proton at H-8 in ring A. The observed
long-range correlation of two O-methyl protons at δ 3.79 (3H,
s, OCH3) to C-6 (δ 139.9) and δ 3.95 (3H, s, OCH3) to C-7 (δ
158.2) in the HMBC indicated the location of the two methoxy
groups at C-6 and C-7, respectively. The aglycone obtained
from the acid hydrolysis of 1 was identified as cirsimaritin (4)
by comparison of NMR data with those in literature [3],
indicative of 1 a cirsimaritin glucoside. The glucosyl moiety
was determined to be attached at the C-5 hydroxyl group due
to an upfield shift of the C-5 signal from δ 152.1 in 4 [3] to δ
148.2 in 1, and was confirmed by the observed correlation
between H-1″ and C-5 in the HMBC spectrum. The coupling
constant of H-1″ (δ 4.77, d, J=7.6 Hz) suggested a β-anomeric
configuration for the glucosyl and its D-configuration was
determined via GC analysis of chemical derivatives of the
β-anomeric configurations for the two glucosyl moieties were
assigned based on the coupling constants of H-1″ (δ 4.79, d,
J=8.0 Hz) and H-1‴ (J=7.6 Hz). The D-configuration glucose
in 2 was determined in the same manner as that described for
1. Therefore, the new isolate 2 was identified as 5, 4′-O-β-D-
diglucopyranosyl cirsimaritin.
To investigate the anti-inflammatory effect, the isolated
compounds 1–7 were incubated at 20 and 40 μg/mL with
lipopolysaccharide (LPS)-activated RAW 264.7 cells for
24 h. Compound 6 displayed potent activity against nitrite
production in macrophages induced by LPS (100 ng/mL),
while 4 and 7 were moderately active, 2, 3, and 5 weakly
active, and 1 inactive (Table 2). In addition, these compounds
were tested for cytotoxicity against three human cancer cell
lines, Hep G2, COLO-205, and HL-60. The results showed that
2, 4, 6, and 7 exhibited moderate anti-proliferative activity
against COLO-205 cells with IC50 values of 7.1, 13.1, 6.1, and
6.8 μM, respectively. Compounds 1–7 were inactive against
the other two cell lines (Table 3).
Acknowledgement
glucose of
1 obtained by acid hydrolysis and the
same derivative of standard D-glucose. Thus, 1 was identified
as 5-O-β-D-glucopyranosyl cirsimaritin based on the above
spectroscopic data and chemical analysis.
The authors wish to thank Naturex, Inc. for the financial
assistance in this study.
The HRESIMS of 2 displayed protonated molecular ion at
m/z 639.1929 [M+H]+, suggesting a molecular formula of
C29H34O16. The IR and UV spectra of 2 were merely identical
to those of 1. The 13C NMR spectrum of 2 displayed very
similar signals to those of 1, specifically a flavone with two
methoxy groups (δ 56.6 and 60.8), but with two glucopy
ranosyl units (Table 1). The two methoxy groups and one
glucosyl were determined at C-6, C-7, and C-5 positions,
respectively by the observed correlations of the two O-methyl
protons and anomeric H-1″ to C-6, C-7, and C-5, respectively
in HMBC (Table 1). It was thus suggested that 2 had the same
skeleton as 1, and the site of the remaining glucopyranosyl
moiety was considered at the C-4′ hydroxyl group by the
comparison of the 13C NMR data of the B-ring between 2 and
cirsimarin (4′-O-cirsimaritin glucopyranoside, 3), where
similar chemical shifts of C-1′ to C-6′ were found between 1
and 3 [3]. The direct evidence came from the observed long-
range H–C correlation of H-1‴ (δ 5.03, d, J=7.6 Hz) to C-4′
(δ 160.1) in the HMBC spectrum and NOE correlation of H-1‴
to H-3′, H-5′ (δ 7.19, d, J=8.8 Hz) in the ROESY spectrum. The
References
[1] Hasrat JA, De Backer JP, Vauquelin G, Vlietinck AJ. Medicinal plants in
Suriname: screening of plant extracts for receptor binding activity.
Phytomedicine 1997;4:59–65.
[2] Hasrat JA, De Bruyne T, De Backer JP, Vauquelin G, Vlietinck AJ.
Cirsimarin and cirsimaritin, flavonoids of Microtea debilis (Phytolac-
caceae) with adenosine antagonistic properties in rats: leads for new
therapeutics in acute renal failure.
1150–6.
J Pharm Pharmacol 1997;49:
[3] Hasrat JA, Pieters L, Claeys M, Vlietinck A, De Backer JP, Vauquelin G.
Adenosine-1 active ligands: cirsimarin, flavone glycoside from
Microtea debilis. J Nat Prod 1997;60:638–41.
[4] Girotti C, Ginet M, Demarne FC, Lagarde M, Géloën A. Lipolytic activity
of cirsimarin extracted from Microtea debilis. Planta Med 2005;71:
1170–2.
[5] Soulage C, Soares AF, Girotti C, Zarrouki B, Demarne FE, Lagarde M,
et al. Antioxidant effect of cirsimarin, a flavonoid extracted from
Microtea debilis. In: Govil JN, Singh VK, Mishra SK, editors. Recent
Progress in Medicinal Plants, Vol. 20. Houston: Studium Press LLC;
2008. p. 55–63.
[6] Chari VM, Grayer-Barkmeijer RJ, Harborne JB, Österdahl BG. An acylated
allose-containing 8-hydroxyflavone glycoside from Veronica filiformis.
Phytochemistry 1981;20:1977–9.
a

172
N. Bai et al. / Fitoterapia 82 (2011) 168–172
[7] Wollenweber E, Wassum M. Salvigenin und ein neues naturliches
[10] Powell RG, Weisleder D, Smith CR, Boettner FE. Drummondones A and
B: unique abscisic acid catabolites incorporating a bicyclo[2.2.2]octane
ring system. J Org Chem 1986;51:1074–6.
flavon aus den knospen von Alnus japonica. Tetrahedron Lett 1972;13:
797–800.
[8] Sakakibara M, DiFeo Jr D, Nakatani N, Timmermann B, Mabry TJ.
Flavonoid methyl ethers on the external leaf surface of Larrea tridentata
and L. divaricata. Phytochemistry 1976;15:727–31.
[11] Mosmann J. Rapid colorimetric assay for cellular growth and survival:
application to proliferation and cytotoxicity assays. J Immunol Meth
1983;65:55–63.
[9] Galbraith MN, Horn DHS. Structures of the natural products blumenols
A, B, and C. J Chem Soc Chem Commun 1972;3:113–4.