Copyright 2006 John Wiley & Sons, Ltd.

Phytother. Res
.
21
, 3236 (2007)
DOI: 10.1002/ptr

32

M. R. LOIZZO
ET AL.

Copyright 2006 John Wiley & Sons, Ltd.

PHYTOTHERAPY RESEARCH
Phytother. Res.
21
, 3236 (2007)
Published online 27 October 2006 in Wiley InterScience
(www.interscience.wiley.com)
DOI
: 10.1002/ptr.2008

Inhibition of Angiotensin Converting Enzyme

(ACE) by Flavonoids isolated from
Ailanthus

excelsa
(Roxb) (Simaroubaceae)
Monica Rosa Loizzo
1

*, Ataa Said
2

, Rosa Tundis
1

, Khaled Rashed
2

, Giancarlo Antonio
Statti
1

, Antje Hufner
3

and Francesco Menichini

1
1

Department of Pharmaceutical Sciences, University of Calabria, Rende (CS), Italy

2

National Research Centre, Pharmacognosy Department, Dokki, Cairo, Egypt

3

Institute for Pharmaceutical Chemistry and Pharmaceutical Technology, University of Graz, Schubertstr.1, A8010
Graz, Austria

In our screening program for antihypertensive properties of plants, the leaves of

Ailanthus excelsa
(Roxb), a
plant used in Egyptian traditional medicine, were analysed. Chromatographic separation of
A. excelsa
MeOH
extract yielded six flavonoids for the first time from this species, namely apigenin, luteolin,
kaempferol-3O

arabinopyranoside, kaempferol-3O

-galactopyranoside, quercetin-3O

-arabinopyranoside and luteolin-7O

-glucopyranoside. The
in vitro
hypotensive activities of the MeOH extract and the isolated compounds
were elucidated. All the flavonoids tested exhibited ACE inhibitory activity, in particular the
most active
compound was kaempferol-3O

-galactopyranoside with an IC
50

value of 260

. Copyright 2006 John

Wiley & Sons, Ltd.

Keywords:
Ailanthus excelsa
(Roxb); flavonoids; angiotensin converting enzyme (ACE); hypertension.
Received 29 May 2006
Revised 3 July 2006
Accepted 13 August 2006
* Correspondence to: Dr M. R. Loizzo, Department of Pharmaceutical
Sciences, University of Calabria, 87036 Rende (CS), Italy.
E-mail: mr.loizzo@unical.it

function (Miller
et al.
, 1994). However, the side effects
such as cough and angioneurotic edema associated
with clinically used ACE inhibitors have been reported
(Israili and Hall, 1992). Thus, the screening and development of new ACE inhibitors would be beneficial
in the treatment of cardiovascular disease without side
effects.

As a part of our research for a natural therapeutic

approach to the treatment of high blood pressure,
in vitro
screening has been conducted to evaluate the
ACE inhibition of the MeOH extract and flavonoids
from the leaves of
Ailanthus excelsa
(Roxb). A number
of screening studies on plants (Anderson and Anderson,
1997; Nyman
et al.
, 1998; Duncan
et al.
, 1999; Oh
et al.
,
2002) and a natural class of compounds such as
alkaloids (Oh
et al.
, 2003), xanthones (Chen and Lin,
1992), terpenoids (Morigiwa
et al.
, 1986; Hansen
et al.
,
1996), fatty acids (Morota
et al.
, 1987), peptides (Wagner
et al.
, 1991), hydrolysable tannins (Ueno
et al.
, 1988),
proanthocyanidins (Kang
et al.
, 2003), flavonoids
(Kameda
et al.
, 1987; Actis-Goretta
et al.
, 2003; Oh
et al.
, 2004) have been reported to exert ACE inhibition activity.
Ailanthus
is a deciduous tree belonging to the family
Simaroubaceae and is widely distributed in Asia and
north Australia. Its native origin is China and it is known
as tree of heaven, tree of sun or Persian sumach

(Adamik and Brauns, 1957). The two main

Ailanthus
species which are cultivated abundantly in Egypt are
A.
altissima
(Mill.) Swingle and
A. excelsa
(Roxb). In
traditional medicine
A. excelsa
is used to cure wounds
and skin eruptions and is used in the indigenous system
of medicine as a antipyretic, and for bronchitis, asthma
and in conditions of diarrhoea and dysentery (British
Pharmacopoeia, 1988).
INTRODUCTION
Hypertension is a common and often progressive disorder that possesses a major risk for cardiovascular and
renal disease. Recent data have revealed that the global burden of hypertension is an important and increasing public health problem worldwide and that the level
of awareness, treatment and control of hypertension
varies considerably among countries (Kearney
et al
.,
2005). Hypertension is often called a silent killer
because persons with this pathological condition can
be asymptomatic for years and then have a fatal heart
attack or stroke. Most persons (90%95%) with high
blood pressure have essential hypertension, for which
the cause cannot be determined, and as a result, treatment is not specific (Mann and Oddon, 2001). The
reninangiotensin system plays a relevant role in the
regulation of an organisms water, electrolytes and
blood. ACE is a cell membrane peptidase, working as
an ectoenzyme, with its catalytic site exposed at the
extracellular surface of the cell. It catalyses the conversion of angiotensin I into the active vasoconstrictor
octapeptide, angiotensin II (Brown and Hall, 2005).
Angiotensin converting enzyme (ACE) inhibitors are
widely used for the treatment of cardiovascular disease
since they improve blood pressure, control patients with
hypertension and prolong survival in patients with acute
myocardial infarction (Shlipak
et al.
, 2001), asymptomatic left ventricular dysfunction (Borghi
et al.

, 2005),
congestive heart failure (Carson, 2000) and renal dysINHIBITION OF ACE BY
AILANTHUS EXCELSA

33

Copyright 2006 John Wiley & Sons, Ltd.

Phytother. Res
.
21
, 3236 (2007)
DOI: 10.1002/ptr

Previous phytochemical studies on

A. excelsa
have
demonstrated the presence of quassinoids, alkaloid,
terpenoids and proteins (Ogura
et al.
, 1977; Joshi
et al
.,
2003a; Sherman
et al.
, 1980; Nag and Matai, 1994).
A.
excelsa
extracts and some isolated compounds have
demonstrated medicinal properties such as significant
antileukemic, antibacterial, antifungal and antifertility
activities (Ogura
et al
., 1977; Dhanasekaran
et al.
, 1993;
Shrimali
et al.
, 2001; Joshi
et al
., 2003b).
MATERIALS AND METHODS
General.
The NMR (
1

H- and
13

C-NMR) spectra were

recorded at 400 MHz and at 100 MHz, respectively,
on a Varian Unity Inova-400 (297) 5 mm tubes. The

values are reported as ppm relative to TMS in DMSOd

6 and
J
values are given in Hz.
Chemicals.
Chemicals and reagents, used for the study
of antihypertensive activity, were purchased from SigmaAldrich Co. (Milan, Italy) while other chemicals,
solvents and reagents used in chromatography were
purchased from Merck, Egypt.
Plant material.
A. excelsa
(Roxb) leaves were collected
from the Zoo Garden, Giza, Egypt. The plant material
was identified by Dr Kamal El-Batanony, Professor of
Taxonomy and Botany, Faculty of Science, Cairo University. A voucher specimen was deposited in the NRC
herbarium.
Extraction and isolation.
Powdered, air dried leaves of
A. excelsa
(1 kg) were extracted with methanol (70%)
in a Soxhlet apparatus and evaporated to dryness to
give 106.5 g. The residue was dissolved in 1 L of distilled water and then extracted with petroleum ether,
chloroform and ethyl acetate, respectively. Each fraction was dried over anhydrous sodium sulphate and
concentrated under reduced pressure to give 29 g of
petroleum ether, 14 g of chloroform and 10.5 g of ethyl
acetate fractions, respectively. The bioactive ethyl acetate fraction was subjected to column chromatography using silica gel (E. Merck, type 60230 mesh, 300 g)
as adsorbent and elution was carried out with chloroform followed by gradually increasing polarity with
methanol. Elution with CHCl
3

:MeOH mixture 98:2

afforded two fractions A and B. Elution with
CHCl
3

:MeOH mixture 95:5 and 90:10 afforded fraction

C and fraction D, respectively. Fractions E and F were
obtained using the eluent CHCl
3

:MeOH 85:15. Elution

and fractionation processes were controlled by UV-light
and exposure to ammonia vapour.
Fractions AD were chromatographed over Sephadex
LH-20 using water for elution, to afford one flavonoid
for each fraction: apigenin (

1
,
15 mg), luteolin (
2
, 25 mg),
kaempferol-3O
-

-arabinopyranoside (
3
, 85 mg) and
kaempferol-3O
-

-galactopyranoside (
4
, 35 mg). Pure
compounds quercetin-3O
-

-arabinopyranoside (
5
,
85 mg) and luteolin-7O
-

-glucopyranoside (
6
, 85 mg)
were obtained by column chromatography fractionation
of E and F, respectively, on microcrystalline cellulose
(with water as eluent with gradually increasing amounts
of methanol) and Sephadex LH-20 using water for
elution.
Apigenin (1).
1

H NMR (400 MHz, DMSO-d6):

12.93
(1H, s, 5-OH), 7.90 (2H, d,
J
=
9.0 Hz, H-2

and H-6

),
6.92 (2H, d,
J
=
9.0 Hz, H-3

and H-5

), 6.76 (1H, s, H3), 6.49 (1H, d,

J
=
2.0 Hz, H-8), 6.19 (1H, d,
J
=
2.0 Hz,
H-6).
13

C NMR (100 MHz, DMSO-d6):

180.7 (C-4),
164.2 (C-7), 163.2 (C-2), 162.0 (C-4

), 161.3 (C-5), 157.9

(C-9), 128.2 (C-2

and C-6

), 120.9 (C-1

), 116.0 (C-3

and C-5

), 103.6 (C-10), 102.4 (C-3), 98.9 (C-6) and 94.2

(C-8).
Luteolin (2).
1

H NMR (400 MHz, DMSO-d6):

13.0 (1H, s, 5-OH), 7.40 (1H, dd,

J
=
2.2, 7.8 Hz,
H-6

), 7.39 (1H, d,

J
=
2.2 Hz, H-2

), 6.88 (1H, d,
J
=
7.6 Hz, H-5

), 6.65 (1H, s, H-3), 6.43 (1H, d,

J
=
2.0 Hz, H-8), 6.18 (1H, d,
J
=
2.0 Hz, H-6).
13

C
NMR (DMSO-d6, 100 MHz): 181.7 (C-4), 164.2 (C-7),
164.0 (C-2), 161.6 (C-5), 157.4 (C-9), 149.8 (C-4

), 145.9
(C-3

), 121.6 (C-1

), 119.1 (C-6

), 116.2 (C-5

), 113.5
(C-2

), 103.8 (C-10), 102.7 (C-3), 98.6 (C-6), 94.0

(C-8).
Kaempferol-3O
-

-arabinopyranoside (3).
1

H-NMR
(400 MHz, DMSO-d6)

12.65 (1H, s, 5-OH), 8.08 (2H,

d,
J
=
8.8 Hz, H-2

and H-6

), 6.88 (2H, d,
J
=
8.4 Hz, H3

and H-5

), 6.42 (d,
J
=
2.0 Hz, H-8), 6.19 (d,
J
=
2.0 Hz, H-6), 5.33 (d,
J
=
5.2 Hz, H1

), 3.65 (1H, m, H4

), 3.74 (1H, dd,

J
=
5.3, 6.0 Hz, H-2

), 3.56 (1H, dd,

J
=
5.8, 11.6 Hz, H-5

), 3.52 (1H, dd,

J
=
2.7, 6.9 Hz, H3

), 3.19 (1H, dd,

J

=
2.0, 11.6 Hz, H-5

).
13

C NMR
(DMSO-d6, 100 MHz)

177.6 (C4), 164.9 (C7), 161.3

(C5), 160.1 (C4

), 156.5 (C2, C9), 133.6 (C3), 131.0 (C2

,
C6

), 120.8 (C1

), 115.3 (C3

, C5

), 103.9 (C10), 101.4

(C1

), 98.9 (C6), 93.8 (C8), 64.3 (C5

), 71.7 (C3

), 70.9
(C2

), 66.1 (C4

).
Kaempferol-3O
-

-galactopyranoside (4).
1

H-NMR
(400 MHz, DMSO-d6)

12.57 (1H, s, 5-OH), 8.04 (2H,

d,
J
=
8.9 Hz, H-2

and H-6

), 6.88 (2H, d,
J
=
8.9 Hz, H3

and H-5

), 6.44 (d,
J
=
2.1 Hz, H-8), 6.21 (d,
J
=
2.1 Hz, H-6), 5.34 (d,
J
=
7.8 Hz, H1

), 3.65 (1H, s, H4

), 3.54 (1H, t,
J
=
8.9 Hz, H-2

), 3.45 (1H, dd,

J
=
5.5,
9.6 Hz, H-6

), 3.37 (1H, dd,

J
=
2.8, 9.8 Hz, H-3

), 3.33
(1H, m, H-5


), 3.29 (1H, m, H-6

).
13

C-NMR (100 MHz,

DMSO-d6)

177.7 (C4), 164.5 (C7), 161.2 (C5), 160.0

(C4

), 156.7 (C2, C9), 133.0 (C3), 130.9 (C2

, C6

), 121.1
(C1

), 115.2 (C3

, C5

), 104.1 (C10), 101.9 (C1

), 99.3
(C6), 93.8 (C8), 75.6 (C5

), 73.7 (C3

), 71.2 (C2

), 67.8
(C4

), 60.5 (C6

).
Quercetin-3O
-

-arabinopyranoside (5).
1

H NMR
(400 MHz, DMSO-d6)

12.65 (1H, s, 5-OH), 7.66 (1H,

dd,
J
=
2.2, 8.0 Hz, H-6

), 7.50 (1H, d,
J
=
2.3 Hz, H2

),
6.83 (1H, d,
J
=
8.6 Hz, H5

), 6.38 (1H, d,
J
=
2.3 Hz,
H-8), 6.18 (1H, d,
J
=
2.3 Hz, H-6), 5.26 (1H, d,
J
=
5.3 Hz, H-1

), 3.75 (1H, dd,

J
=
5.0, 6.8 Hz, H-2

), 3.63
(1H, m, H-4

), 3.60 (1H, d,
J
=
5.9, 11.3 Hz, H-5

), 3.51
(1H, dd,
J
=
2.8, 6.8 Hz, H-3


), 3.21 (2H, d,
J
=
11.3 Hz,
H-5

).
13

C NMR (100 MHz, DMSO-d6)

177.65 (C4),
164.54 (C7), 161.37 (C5), 156.3 (C2), 156.39 (C9), 148.79
(C4

), 145.16 (C3

), 133.90 (C3), 122.17 (C6

), 121.04
(C1

), 115.93 (C2

), 115.54 (C5

), 104.00 (C10), 101.58

(C1

), 98.86 (C6), 93.67 (C8), 71.81 (C1

), 70.88 (C2

),
66.20 (C4

), 64.39 (C5

).
Luteolin-7O
-

-glucopyranoside (6).
1

H NMR
(400 MHz, DMSO-d6):

12.98 (1H, s, 5-OH), 7.43 (1H,

Copyright 2006 John Wiley & Sons, Ltd.
Phytother. Res
.
21
, 3236 (2007)
DOI: 10.1002/ptr

34
M. R. LOIZZO
ET AL.

dd,
J
=
2.2, 8.0 Hz, H-6

), 7.41 (1H, d,
J
=
7.8 Hz, H-2

),
6.88 (1H, d,
J
=
7.6 Hz, H-5

), 6.72 (1H, s, H-3), 6.78

(1H, d,
J
=
2.0 Hz, H-8), 6.43 (1H, d,
J
=
2.0 Hz, H-6),
5.07 (1H, m, H-1

), 3.7 (1H, d,
J
=
11.7, H-6

), 3.47 (1H,
m, H-6

), 3.44 (1H, m, H-5

), 3.28 (1H, m, H-3

), 3.25
(1H, m, H-2

), 3.17 (1H, t,
J
=
7.3, H-4

).
13

C NMR
(DMSO-d6, 100 MHz): 181.9 (C-4), 163.8 (C-7), 164.7
(C-2), 161.3 (C-5), 157.1 (C-9), 150.6 (C-4

), 146.1 (C3

), 121.1 (C-1

), 119.3 (C-6

), 116.2 (C-5

), 113.6 (C-2

),
105.5 (C-10), 103.1 (C-3), 99.6 (C-6), 94.8 (C-8), 100.1
(C-1

), 77.3 (C-5

), 76.56 (C-3

), 73.28 (C-2

), 69.73 (C4

), 60.79 (C-6

).
Bioassay procedures for ACE inhibition.
The
in vitro
ACE inhibitory activity was measured using the
method described by Elbl and Wagner (1991), which
was later modified by Hansen

et al.
(1995). Briefly, the
chromophore-fluorophore labelled substrate dansyltriglycine was cleaved by an angiotensin I-converting
enzyme preparation from rabbit lung (EC 3.4.15.1)
into dansylglycine, which is quantitatively measured by
HPLC. 1 mg of MeOH extract and isolated compounds
was dissolved in 1 mL HEPES assay buffer, to obtain a
final concentration of 330

g/mL.
The ACE solution
(25

L) was preincubated with a test or control solution (25

L) for 5 min at 37 C. The enzyme reaction

was started by adding a combined solution (25

L) of
the substrate dansyltriglycine (7.86 m
M

) and the internal standard, dansylL

-glutamine (0.353 m
M

) for a time
of incubation chosen by plotting a calibration curve.
The reaction was stopped by adding a solution of 0.1
N

Na
2

EDTA (50

L). The dansylglycine was quantified

by reversed phase HPLC with UV detection at 250 nm.
Instrumentation: HPLC Perkin Elmer Series 410 LC
pump; injector: Perkin Elmer 20

L loop; detector:
Perkin Elmer UV/VIS LC290 spectophotometric;
solvent system: Altech SN 1250-99, Part. N 288215 BIN
II 43; chromatographic column type: Hypersil ODS 5 u
Lot N 5002.150 mm

4.6 m
M

SN:1250-99; mobile phase:

isocratic system 10 m
M

NaH
2

PO
4

buffer (pH 7):

acetonitrile (88:12); flow rate 2 mL/min, run time 30 min.
The linear calibration curve for dansylglycine was plotted from 0.2 to 25

g/mL. All materials were purchased

from Sigma-Aldrich, Italy.
The decreased concentration of dansylglycine in the test reaction compared with
the control reaction was expressed as the percentage
inhibition and calculated from the equation:
Inhibition
dansylglycine T
dansylglycine C
(%)
()
()
=
100 100
where T is the test reaction and C is the control
reaction.
The therapeutic drug captopril was used as a
reference ACE inhibitor. All experiments were carried
out in triplicate. Data were expressed as mean

SD.
Differences were evaluated by one-way analysis of
variance (ANOVA) test completed by a multicomparison Dunnetts test. Differences were considered
significant at
p
<
0.01.
The inhibitory concentration 50%
(IC
50

) was calculated from a dose-response curve obtained by plotting the percentage inhibition versus the
concentrations with the use of GraphPad Prism 4.0
Software.
RESULTS AND DISCUSSION
As a part of our search for a therapeutic approach
for the treatment of high blood pressure, a MeOH

extract of
A. excelsa
leaves was screened for its inhibitory effect on ACE with 53.78% inhibition at the
screened concentration of 330

g/mL.
The bioactive ethyl acetate fraction of
A. excelsa
was
chromatographed on silica gel followed by successive
separation on Sephadex LH-20 and cellulose affording
six pure known flavonoids identified as apigenin, luteolin,
kaempferol-3O
-

-arabinopyranoside, kaempferol-3O
-

-galactopyranoside, quercetin-3O
-

-arabinopyranoside
and luteolin-7O
-

-glucopyranoside. All the structures

were determined on the basis of the spectral data (
1

HNMR,
13

C-NMR and 2D COSY, HSQC, HMBC), identical with those previously described (Nakasugi and
Komai, 1998; Sanbongi
et al.
, 1998; Yun-Lian
et al.
, 2000;
Foo
et al.
, 2000; Flamini
et al.
, 2001). Several flavonoids

have been reported to inhibit ACE activity by 60%

90% at a concentration of 330

g/mL (Lacaille-Dubois
et al
., 2001; Kameda
et al.
, 1987; Wagner, 1993).
Isolated compounds inhibited the ACE activity in a
dose-dependent manner (Fig. 1), and the IC
50

values
are reported in Table 1. The most active compound
was kaempferol-3O
-

-galactopyranoside with an IC
50

of 260

while kaempferol-3O
-

-arabinopyranoside
showed an inhibition of 320

.
The arabinosyl moiety seemed to have a negative
influence on the ACE inhibition, in fact quercetin-3O
-

-arabinopyranoside also showed a value of inhibition

less high than the other compounds (IC
50

310

).
Luteolin exhibited an IC
50

of 290

, the introduction
of glucopyranoside moiety in position 7 weakly reduced
the flavonoid activity (IC

50

280

) while apigenin
showed an IC
50

value of 280

on ACE activity.
Our data are in accordance with previous work of Oh
et al.
(2004) that reported the ACE inhibitory activity
of five flavonoids with IC
50

values ranging from 158.9 to

708.8

.
Polyphenolic substances such as flavonoids exert a
great variety of physiological actions and are held partly
responsible for the favourable health properties of
some food, including a reduced risk of cardiovascular
diseases. An increasing number of epidemiological
and experimental studies have established a positive
correlation between the consumption of foods and
supplements rich in flavonoids or phytomedicine preparation, and protection against atherosclerosis and
cardiovascular diseases. In addition, flavonoids inhibit
Table 1. Angiotensin converting enzyme inhibitory activity of
flavonoids from
A. excelsa
(Roxb) leaves
Compound IC
50

)
Apigenin 280

3.2
a

Luteolin 290

2.9
a

Kaempferol-3O

-arabinopyranoside 320

4.1

Kaempferol-3O

-galactopyranoside 260

3.0
a

Quercetin-3O

-arabinopyranoside 310

2.2
a

Luteolin-7O

-glucopyranoside 280

3.4
a

Captopril 0.02

0.0004
IC
50

values are mean

SEM (
n
=
3);
a

p
<
0.01 vs control.
INHIBITION OF ACE BY
AILANTHUS EXCELSA

35

Copyright 2006 John Wiley & Sons, Ltd.

Phytother. Res
.
21
, 3236 (2007)
DOI: 10.1002/ptr

Figure 1.
Dose-dependent inhibition of ACE by isolated flavonoids from
A. excelsa
.
(
1)
apigenin, (
2
) luteolin, (
3
) kaempferol-3O


arabinopyranoside, (
4
) kaempferol-3O

-galactopyranoside, (
5
) quercetin-3O

-arabinopyranoside, (
6
) luteolin-7O

-glucopyranoside.
Each data point represents the mean

SD (
n
=
3).

lipid peroxidation (LPO), platelet aggregation and

activity of enzyme systems including cyclooxygenase
and lipoxygenase, and reduce the capillary permeability and fragility. Flavonoid preparations have been used
widely in medical practice for over 40 years to treat
disorders of the circulation. Over 100 preparations containing this class of natural compounds, including hesperidine, rutin and diosmetin are marketed in Europe
(Jaeger
et al.
, 1988).
Flavonoids exert these effects as antioxidants, free
radical scavengers and chelators of divalent cations
(Cook and Samman, 1996).
The biological mechanisms by which flavonoids modulate vascular function and blood pressure appear to
be associated with the action of nitric oxide (NO).
Although the initial events leading to an increased
production of NO are not totally identified, it is
accepted that regulation of the reninangiotensin
system in endothelial cells could be involved in the
control of NO production (de Cavanagh
et al.
,
2004).

ACE, a crucial enzyme in the regulation of the renin

angiotensin system, is a zinc-containing peptidyl
dipeptide hydrolase (Strittmatter and Snyder, 1986). The
active site of ACE is known to consist of three parts: a
carboxylate binding functionality such as the guanidinium group of arginine, a pocket that accommodates
a hydrophobic side chain of
C
-terminal amino acid
residues and a zinc ion. The zinc ion coordinates to
the carbonyl of the penultimate peptide bond of the
substrate, whereby the carbonyl group becomes polarized and is subjected to a nucleophilic attack. Therefore, some flavonoids (Wagner
et al.
, 1991) were
suggested to show
in vitro
activity via the generation
of chelate complexes within the active centre of ACE.
Free hydroxyl groups of phenolic compounds are also
suggested to be important structural moieties to chelate
the zinc ions, thus inactivating the ACE activity (Chen
and Lin, 1992).
Since compounds
1

6
contain aromatic hydroxyl
groups, these free hydroxyl groups may due to the generation of chelate complexes with zinc ions within the
active centre of the enzyme.
Our data demonstrated that flavonoids isolated from
A. excelsa
leaves have similar levels of inhibitory activity toward ACE compared with previously reported
ACE inhibitory flavonoids.
Further work is needed to clarify the mechanism of
ACE inhibition and the relevance of these flavonoids
to the purported antihypertensive activity of the
A.
excelsa.
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