ORIGINAL ARTICLE
Cardioprotective Effects of Sesbania grandiflora in
Cigarette Smoke–exposed Rats
Thiyagarajan Ramesh, PhD, Ramalingam Mahesh, PhD, Chandrabose Sureka, PhD,
and Vavamohaideen Hazeena Begum, PhD
Abstract: Cigarette smoke is a major risk factor of coronary heart
disease, myocardial infarction, and cardiac death. It has been reported
to contain large amounts of oxidants. This study was undertaken
to evaluate the cardioprotective effects of Sesbania grandiflora
(S. grandiflora) against cigarette smoke–induced oxidative damage in
rats. Adult male Wistar-Kyoto rats were exposed to cigarette smoke
for a period of 90 days and consecutively treated with S. grandiflora
aqueous suspension (SGAS, 1000 mg/kg body weight per day orally)
for a period of 3 weeks. Lactate dehydrogenase activity in serum and
cardiac lipid peroxidation product level were significantly increased
while the activities of cardiac superoxide dismutase, catalase,
glutathione peroxidase, glutathione reductase, glutathione-S-trans-
ferase, and glucose-6-phosphate dehydrogenase then the levels of
reduced glutathione, vitamin C, and vitamin E were significantly
decreased in rats exposed to cigarette smoke. Besides, copper level
was elevated, whereas zinc, manganese, and selenium levels were
significantly diminished in the heart of rats exposed to cigarette
smoke. Treatment with SGAS restored the antioxidant status and
retained the levels of micronutrients. These results suggest that
chronic cigarette smoke exposure increases the oxidative stress,
thereby disquieting the cardiac defense system and S. grandiflora
protects the heart from the oxidative damage through its antioxidant
potential.
Key Words: antioxidant, cigarette smoke, lipid peroxidation, heart,
micronutrients, Sesbania grandiflora
(J Cardiovasc Pharmacol TM 2008;52:338–343)
C igarette smoking increases the risk of coronary heart
disease (CHD), myocardial infarction, and cardiac death.
An analysis of recent epidemiological studies showed that
passive smoking increases the risk of CHD by 25%.1 Thus, the
heart disease risk of a passive smoker is almost half of the risk
of an active smoker, even if the quantity of inhaled smoke is
only 1% of that coming from a daily pack of cigarettes.1
Furthermore, it has been suggested that in nonsmokers, even
a short period (10–30 min) of exposure to cigarette smoke is
Received for publication May 3, 2008; accepted July 28, 2008.
From the Department of Siddha Medicine, Faculty of Science, Tamil
University, Thanjavur-613010, Tamil Nadu, India.
The authors declare no conflicts of interest.
Reprints: Dr. T. Ramesh, PhD, Division of Cardiology, Department of Internal
Medicine, Seoul National University College of Medicine, 28 Yongon-dong.
Chongno-gu, Seoul 110-744, South Korea (e-mail: thiyagaramesh@
gmail.com).
Copyright Ó 2008 by Lippincott Williams & Wilkins
338
enough to induce platelet aggregation, endothelial damage,
endothelial dysfunction, and measurable changes in antiox-
idant defense and lipid peroxidation2,3 due to the toxic
constituents of cigarette smoke.
Cigarette smoke contains high concentrations of two
different populations of free radicals, one in the tar component
and the other in the gas component phase of smoke.4 About
4700 constituents of mainstream cigarette smoke have been
identified5; thus tobacco smoke causes a mixed oxidative
challenge to the cells. Free radicals, as reactive species of
oxygen, induce the functional and structural damages of
cardiac myocytes and may play an important role in diverse
acute coronary syndromes and heart failure, in which an
imbalance of oxidative stress status is present.6 Smoking may
enhance oxidative stress not only through the production of
reactive oxygen radicals in smoke but also through weakening
of the antioxidant defense mechanisms. Antioxidants consti-
tute the primary defense system that limit the toxicity
associated with cigarette smoke induced free radicals. Hence,
these antioxidants mainly enzymic antioxidants such as
superoxide dismutase (SOD), catalase (CAT), glutathione
peroxidase (GPx), and glutathione-S-transferase (GST) and
nonenzymic antioxidant like reduced glutathione (GSH) were
expected to be consumed by enhanced radical reactions.7 Bio-
logical compounds with antioxidant properties contribute to
the protection of cells and tissues against deleterious effects of
cigarette smoke generated reactive oxygen species (ROS) and
other free radicals.8 Experimental studies have suggested
a protective role for micronutrients, vitamins, and antioxidants
of natural origin in modifying the major diseases related to
cigarette smoking. Hence, the current study was planned to
evaluate the cardioprotective effects of S. grandifora on
cigarette smoke–exposed rats.
Sesbania grandiflora L. pers (Febaceae), commonly
known as sesbania and agathi, has been used as an important
dietary nutritive source in Southeast Asian countries. S.
grandiflora leaves are the richest source of amino acids,
minerals and vitamins (vitamin A, vitamin C, thiamine,
riboflavin, and nicotinic acid).9,10 Various parts of this plant are
used in Indian traditional medicine for the treatment of a broad
spectrum of illness including leprosy, gout, rheumatism and
liver disorders.11,12 It also possess anti-inflammatory, analgesic,
antipyretic, anxiolytic, and anticonvulsive activities.13,14 Our
previous studies reported that S. grandiflora has protective
effect against oxidative damage and hypolipidemic property on
cigarette smoke–exposed rats.15–18 However, the mechanisms
underlying its beneficial effects against smoking-associated
J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008
J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008
diseases are to be fully elucidated. Thus, the present study
has been undertaken to assess the cardioprotective role of
S. grandiflora leaves against oxidative damage in the heart of
rats exposed to cigarette smoke by measuring the level of lipid
peroxidation product and the activities of lactate dehydroge-
nase (LDH), enzymic antioxidants, and also the levels of
nonenzymic antioxidants and micronutrients.
METHODS
Chemicals
Thiobarbituric acid, reduced glutathione, oxidized glu-
tathione, nicotinamide adenine dinucleotide (reduced), nico-
tinamide adenine dinucleotide phosphate, ascorbic acid, and
a-tocopherol were obtained from Sigma Chemical Company
(St. Louis, MO). All other chemicals and reagents used were of
analytical grade with highest purity obtained from Glaxo
Laboratories (Mumbai, India).
Plant Material
Fresh S. grandiflora leaves were collected from a local
plantation (Poovathur, Thanjavur, India). The leaves were
washed thoroughly to remove the contaminants, shade dried,
and powdered finely. The powdered leaves of S. grandiflora
were reconstituted in distilled water to form a suspension.
Thus aqueous suspension of S. grandiflora leaves was
prepared freshly every day prior to the administration.
Experimental Animals
Male Wistar-Kyoto rats weighing 125 to 150 g were
obtained from Venkateshwara Animal Breeding Centre
(Bangalore, India). Animals were housed in polypropylene
cages with filter tops under controlled conditions of a 12-hour
light/dark cycle at 27 6 2°C. All the rats received standard
pellet diet (Amrut rat feed, Pune, India) and water ad libitum.
All animal experiments and maintenance were carried out
according to the ethical guidelines suggested by the Insti-
tutional Animal Ethics Committee.
Experimental Protocol
The animals were divided into four groups of six animals
each: group I (control), administered only vehicle (distilled
water 10 ml/kg body weight per day orally); group II (S.
grandiflora aqueous suspension [SGAS]), administered SGAS
alone (1000 mg/kg body weight per day orally) for a period of
3 weeks; group III (CSE), cigarette smoke–exposed rats; group
IV (CSE+SGAS), cigarette smoke–exposed rats administered
SGAS (1000 mg/kg body weight per day orally) for a period of
3 weeks. Group III and Group IV rats were exposed to
cigarette smoke by modified method of Eun-Mi et al19 as
follows. In this method, the rats were placed in a polypropylene
cage with a lid made of polythene paper. A lighted cigarette
was placed in a flask connected to the cage and air was
supplied into the flask for 10 min by a small air pump. A
length of 5.9 cm of each cigarette was allowed to be burned by
clamping the butt when it was placed in a flask. Each rat was
subjected to inhale the cigarette smoke seven times a day at
regular intervals of an hour (from 11 a.m. to 5 p.m.) for
q 2008 Lippincott Williams & Wilkins
Cardioprotective Role of Sesbania grandiflora
a period of 90 days. Similarly, control rats were exposed to air
instead of smoke.
At the end of the experimental period, the animals were
sacrificed by cervical decapitation. Blood was collected and
separated serum by centrifugation for enzyme analysis. Heart
was isolated, cleaned of adhering fat, and connective tissues.
Known weight of tissue was homogenized in 0.1M tris-HCl
buffer (pH 7.4) containing 0.25 M sucrose and used for the
biochemical estimation.
Biochemical Analyses
The activity of serum LDH was assayed spectrophoto-
metrically according to the standard procedures using
commercially available diagnostic kits. Lipid peroxidation
was estimated by measuring thiobarbituric acid reactive sub-
stances (TBARS) by the method of Beuge and Aust.20 SOD
and CAT activities were assayed by the method of Kakkar
et al21 and Sinha.22 GSH and activities of GSH-related enzymes
such as GPx, GR, GST, and glucose-6-phosphate dehydroge-
nase (G6PDH) were determined by the method of Moron
et al,23 Rotruck et al,24 Stall et al,25 Habig et al,26 and Ellis and
Kirkman27 respectively. Vitamin C and vitamin E were esti-
mated according to the methods of Omaye et al28 and Baker
et al.29 Protein was quantified by the method of Lowry et al.30
Copper (Cu), zinc (Zn), and manganese (Mn) were analyzed
using an atomic absorption spectrophotometer and selenium
(Se) was estimated by coupled atomic emission spectropho-
tometer and fluorometer after digestion of tissue with nitric acid
and perchloric acid.
Statistical Analysis
Results were expressed as means 6 SD (n = 6). The
observed differences were analyzed for statistical significance
by one-way analysis of variance with Tukey’s multiple
comparison as a post-hoc test. Significant P , 0.05, we used
a software for statistical analysis (Graphpad Instat).
RESULTS
Effect of SGAS on Serum LDH Activity in
Cigarette Smoke–Exposed Rats
Figure 1 shows the activity of serum LDH. In cigarette
smoke–exposed rats, the activity of serum LDH was
significantly increased (P , 0.001) when compared with the
control rats. Administration of SGAS to cigarette smoke–
exposed rats showed significant reduction (P , 0.001) in the
activity of serum LDH when compared with the untreated
cigarette smoke–exposed rats. Significant changes were not
observed in the activity of this enzyme in SGAS-only treated
rats.
Effect of SGAS on Lipid Peroxidation in
Cigarette Smoke–Exposed Rats
Cigarette smoke produced a significant elevation in
cardiac TBARS levels in cigarette smoke–exposed rats (P ,
0.001) as compared with control rats. Administration of SGAS
significantly decreased (P , 0.001) the value of TBARS
produced in cigarette smoke–exposed rats as compared with
untreated cigarette smoke–exposed rats. SGAS-only treated
339
Ramesh et al
FIGURE 1. Effect of SGAS on serum LDH activities in control
and cigarette smoke–exposed rats. Values are expressed as
means 6 SD (n = 6). Statistical comparisons were made
between controls vs. SGAS and CSE; CSE vs. CSE+SGAS. *P ,
0.001. NS, nonsignificant.
rats showed no significant changes on TBARS levels when
compared with control rats (Fig. 2).
Effect of SGAS on SOD and CAT Activities in
Cigarette Smoke–Exposed Rats
Cardiac SOD and CAT activities were significantly
decreased (P , 0.001) in cigarette smoke–exposed rats as
compared with control rats. The decreased activities of SOD
and CAT were significantly increased (P , 0.001) after the
SGAS treatment as compared with untreated cigarette smoke–
exposed rats. Significant changes were not observed in the
activities of SOD and CAT in SGAS-only treated rats when
compared with control rats (Fig. 3A and B).
FIGURE 2. Effect of SGAS on cardiac TBARS in cigarette smoke–
exposed rats. Values are expressed as means 6 SD (n = 6).
Statistical comparisons were made between controls vs. SGAS
and CSE; CSE vs. CSE+SGAS. *P , 0.001. NS, nonsignificant.
340
J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008
Effect of SGAS on GSH- and GSH-Related
Enzymes in Cigarette Smoke–Exposed Rats
Cigarette smoke–exposed rats showed significant reduc-
tion in the level of cardiac GSH and activities of GPx, GR,
GST, and G6PDH (P , 0.05 and P , 0.001, respectively) as
compared with control rats. The diminished level of GSH and
activities related to GSH enzymes were significantly increased
(P , 0.001) by SGAS treatment as compared with untreated
cigarette smoke–exposed rats. By the same time, GSH level
and its related enzymes activities were not significantly altered
in SGAS-only treated rats when compared with control rats
(Table 1).
Effect of SGAS on Vitamin C and Vitamin E in
Cigarette Smoke–Exposed Rats
Cardiac vitamin C and vitamin E levels were signifi-
cantly lowered in cigarette smoke–exposed rats (P , 0.001) as
compared with control rats. Administration of SGAS was
restored (P , 0.001) the concentrations of vitamin C and
vitamin E in cigarette smoke–exposed rats when compared
with untreated cigarette smoke–exposed rats. Significant
alterations were not found in the levels of vitamin C and
vitamin E in SGAS-only treated rats as compared with control
rats (Fig. 4A and B).
Effect of SGAS on Micronutrients in Cigarette
Smoke–Exposed Rats
Cu level was significantly elevated while Zn, Mn, and Se
levels were reduced markedly (P , 0.001) in cigarette smoke–
exposed rats when compared with that of the control rats.
These alterations were reverted to near normal after SGAS
treatment with cigarette smoke–exposed rats (P , 0.001).
Significant changes were not observed in the concentrations of
Cu, Zn, Mn, and Se in SGAS-only treated rats when compared
with control rats (Table 2).
DISCUSSION
Cigarette smoke has been identified as a major risk
factor for cardiovascular diseases because the sustained release
of reactive free radicals from the tar and gas phases of smoke
impose oxidative stress, promote lipid peroxidation, and
consequently perturb the antioxidant defense systems in blood
and tissues of smokers.4 Cell membranes being primarily
composed of lipids, especially polyunsaturated fatty acids, are
particularly susceptible to attack by these free radicals from
cigarette smoke, leading to increased permeability and altered
fluidity of the membrane and thereby causing cellular
leakage.31 In the present study, LDH activity was increased
in the serum of cigarette smoke–exposed rats. The increased
activity of LDH is an indication of the severity of cigarette
smoke–induced necrotic damage to the myocardial membrane.
SGAS administration minimized the deleterious effects of
cigarette smoke by maintaining the levels of LDH in serum.
Oxidant balance in the heart has a very important role in
protecting the heart and in allowing normal cardiac contractile
performance. Results from the current study support the
suggestion that the cigarette smoke exposure leads to
important changes in the heart, evidenced by an increase in
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J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008 Cardioprotective Role of Sesbania grandiflora

FIGURE 3. Effect of SGAS on heart of

cigarette smoke–exposed rats. A,
Cardiac SOD activity. Unit of SOD:
50% inhibition of NBT reduction/
min/mg protein. (B) Cardiac CAT
activity. Unit of CAT: mmol of H2O2
decomposed/min/mg protein. Val-
ues are expressed as means 6 SD (n
= 6). Statistical comparisons were
made between controls vs. SGAS
and CSE; CSE vs. CSE+SGAS. *P ,
0.001. NS, nonsignificant.

lipid peroxidation product, mainly TBARS, which is in line
with the observation of previous finding.32 The increased lipid
peroxidation might be a reflection of decreased levels of
enzymatic and nonenzymatic antioxidant defense system.
SOD and CAT are antioxidant enzymes that protect the
cellular constituents against oxidative damage. SOD is the first
enzyme in antioxidant defense that scavenges superoxide
radicals to form H2O2 and hence diminishes the toxic effects of
the radical. In the present study, cardiac SOD activity was
significantly decreased in cigarette smoke–exposed rats. In
addition, cardiac CAT activity, which is involved in the
detoxification of high concentrations of H2O2, also decreased
in cigarette smoke–exposed rats. These results are consistent
with an earlier report.33 Treatment with SGAS significantly
enhanced the activities of cardiac SOD and CAT to near
normal and concomitantly decreased TBARS levels. This
shows the antioxidant potential of the SGAS against cardiac
injury caused by cigarette smoke.
GSH is involved in the protection from dangerous
effects of free radicals, particularly in ischemia. In this study,
cigarette smoke increased the production of free oxygen
radicals and decreased the levels of GSH. Decreased GSH
level may be due to its increased utilization during the burst of
ROS production that protects sulfhydryl group containing
proteins from lipid peroxidation. Our observation is in
correlation with previous finding.33 Besides, the GSH
depletion affects mainly GSH-dependent enzymes such as
GPx, GR and GST making the cells more susceptible to any
further challenge.
GPx is widely distributed in almost all tissues. The
predominant subcellular distribution is in the cytosol and
mitochondrion. This suggests that GPx is the main scavenger
of H2O2 in these subcellular compartments. In the present
study, the cardiac GPx activity was decreased in cigarette
smoke–exposed rats. The observed decreased activity of GPx
with cigarette smoke suggests an increased production of
H2O2 and decreased level of GSH in cigarette smoke–exposed
rats. Administration of SGAS to cigarette smoke–exposed rats
showed that the increased activity of cardiac GPx. The
increased activity of GPx may be due to ameliorated level of
cardiac GSH in cigarette smoke–exposed rats.
GR is an important enzyme for maintaining the
intracellular level of GSH. In this study, the activity of cardiac
GR was found to be decreased in cigarette smoke–exposed
rats. The decreased activity of GR might be mainly due to
depletion of GSH level. Gad and Hassan33 also reported that
the level of GSH which is a substrate of GR was decreased in
the heart of cigarette smoke–exposed rats. SGAS treatment
with cigarette smoke–exposed rats showed increased activity
of cardiac GR by enhancing the level of GSH.
GST is involved in the detoxification of ROS and
tobacco smoke carcinogens, including monohalomethanes,
ethylene oxide, dichloromethane, and the polycyclic aromatic
hydrocarbons from cigarette tar, by conjugating them to
glutathione.34 In this study, the activity of cardiac GST was
found to be decreased in cigarette smoke–exposed rats. The
decreased activity of GST may be due to lowered level of GSH
and elevated level of lipid peroxidation in cigarette smoke–
exposed rats. Administration of SGAS to cigarette smoke–
exposed rats showed increased activity of cardiac GST. The
enhanced activity of GST may be due to increased level of
cardiac GSH in cigarette smoke–exposed rats. In addition, the

TABLE 1. Effect of SGAS on Cardiac GSH- and GSH-Related Enzyme Activities in Cigarette Smoke–exposed Rats
Parameters Control SGAS CSE CSE+SGAS
GSH (mg/mg protein) 3.13 6 0.16 3.48 6 0.12* 2.87 6 0.13† 3.55 6 0.11‡
GPx (mmol GSH oxidized/min/mg protein) 7.17 6 0.67 7.05 6 0.66* 5.53 6 0.44‡ 6.79 6 0.67†
GR (mmol NADPH oxidized/min/mg protein) 0.31 6 0.03 0.33 6 0.03* 0.26 6 0.03§ 0.31 6 0.03§
GST (mmol CDNB-GSH conjugated/min/mg protein) 0.53 6 0.04 0.50 6 0.04* 0.38 6 0.02‡ 0.47 6 0.03‡
G6PDH (U/min/mg protein) 1.24 6 0.06 1.21 6 0.06* 0.94 6 0.05‡ 1.18 6 0.06‡
Values are means 6 SD (n = 6). Statistical comparisons were made between controls vs. SGAS and CSE; CSE vs. CSE1SGAS.
*Not significant.
†P , 0.01.
‡P , 0.001.
§P , 0.05.

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Ramesh et al
Figure 4. Effect of SGAS on hearts
of cigarette smoke–exposed rats. A,
Cardiac vitamin C level (mg/mg
protein). B, Cardiac vitamin E level
(mg/mg protein). Values are
expressed as means 6 SD (n = 6).
Statistical comparisons were made
between controls vs. SGAS and CSE;
CSE vs. CSE+SGAS. *P , 0.001. NS,
nonsignificant.
increased activity of GST may accelerate the reactions of the
ROS and aldehydes with GSH to give less toxic conjugates in
heart.
The enzyme G6PDH is not directly involved in GSH
synthesis but it catalyses the first step in the hexose
monophosphate pathway, the primary pathway that generates
reducing equivalents, NADPH, and thus effectively acts as an
indicator for intracellular redox status.35 NADPH is utilized by
GR to convert oxidized glutathione to reduced glutathione. In
the present study, the activity of cardiac G6PDH was
decreased in cigarette smoke–exposed rats. The decreased
activity of G6PDH led to impairment of GSH regeneration.
SGAS treatment with cigarette smoke–exposed rats showed
increased activity of G6PDH by producing more reducing
equivalents and by the reduction of oxidized glutathione to
reduced glutathione.
Vitamin C has been demonstrated to be an efficient
antioxidant that acts both directly by reaction with aqueous
peroxyl radicals and indirectly by restoring the antioxidant
properties of fat-soluble vitamin E.36 In the present study,
cardiac vitamin C level was decreased in cigarette smoke–
exposed rats. This might be due to increased utilization to
scavenge free radicals, which are released from cigarette
smoke. Administration of SGAS to cigarette smoke–exposed
rats showed increased level of vitamin C. This result proved
that vitamin C, which is present in S. garandiflora, restored the
level of cardiac vitamin C in cigarette smoke–exposed rats.
Vitamin E as an integral part of cell membranes, acts as
cytosolic antioxidant, scavenges the free radicals that promote
peroxidative chain reactions. In the present study, the level of
cardiac vitamin E was decreased in cigarette smoke–exposed
rats. The observed low level of cardiac vitamin E with cigarette
smoke suggests an increased production of free radicals and
TABLE 2. Effect of SGAS on Cardiac Micronutrients in Cigarette Smoke–exposed Rats
Parameters Control
Cu (mg/g) 3.80 6 0.21
Zn (mg/g) 20.00 6 1.04
Mn (mg/g) 1.14 6 0.05
Se (mg/g) 0.31 6 0.02
Values are means 6 SD (n = 6). Statistical comparisons were made between controls vs. SGAS and CSE; CSE vs. CSE+SGAS.
*Not significant.
†P , 0.001.
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J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008
diminished antioxidant level in cigarette smoke–exposed rats.
Decreased cardiac vitamin E level was reverted to near normal
by SGAS treatment on cigarette smoke–exposed rats. This
might be attributed to vitamin C, which is present in SGAS.
Vitamin C is able to regenerate vitamin E.36
Moreover, micronutrients (trace elements) such as Cu,
Zn, Mn, and Se also play major roles in cardiac defense
mechanism. In the present study, cardiac Cu level was
significantly increased in cigarette smoke–exposed rats. The
increased concentration may be related to the delivery of Cu to
the body by cigarettes.37 Notably, the present study demon-
strated a positive and significant correlation between the levels
of Cu and those of lipid peroxidation in cigarette smoke–
exposed rats. It is known that Cu is a powerful catalytic
element, showing a high second-order rate constant in
catalyzing Fenton chemistry reactions and a peculiar capacity
to promote lipid peroxidation.38 The cardiac lipid peroxide
burden represents a remarkable finding, considering the
recognized susceptibility to coronary heart disease. Indeed,
oxidant injury and lipid peroxidation are crucial in myocardial
infarction. Elevated cardiac Cu level was significantly reduced
by SGAS treatment in cigarette smoke–exposed rats.
Zn, Mn, and Se mainly constitute cofactors for various
antioxidant enzymes like SOD and GPx. The present study
showed decreased levels of Zn, Mn, and Se in the heart of rats
exposed to cigarette smoke. This may be due to heavy metals
like cadmium, arsenic, and lead, which are present in cigarette
smoke.39 The heavy metals from cigarette smoke replace the
trace elements that are present in antioxidant enzymes and
decreases the enzyme activities.40 Treatment with SGAS
restored the levels of Zn, Mn, and Se in the heart of cigarette
smoke–exposed rats. Earlier reports showed that mineral
mixture of Ca/P, Zn, and Fe replaced the heavy metals from the
SGAS CSE CSE+SGAS
3.90 6 0.18* 5.10 6 0.21† 4.62 6 0.21†
21.00 6 1.16* 14.00 6 0.76† 18.00 6 1.17†
1.20 6 0.06* 0.63 6 0.03† 0.97 6 0.05†
0.33 6 0.01* 0.12 6 0.02† 0.28 6 0.01†
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J Cardiovasc Pharmacol ä  Volume 52, Number 4, October 2008
body.41 This report is in line with our present results because
S. grandiflora also contains these minerals, which could replace
the heavy metals from the antioxidant enzymes.
In conclusion, the present results indicate that the
cardioprotective effect of SGAS in cigarette smoke–exposed
rats could be related to its antioxidant defense system. Our
results showed that the SGAS was safe and highly effective in
preventing oxidative damage in the heart of rats exposed to
cigarette smoke, possibly due to both antioxidative and
cytoprotective properties. These observations highlight that
the SGAS is one of the promising natural products for
improving defense mechanisms in the physiological systems
against oxidative stress caused by cigarette smoke.
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