Indian Journal of Experimental Biology

Vol. 49, June 2011, pp. 455-460

Hepatoprotective and antioxidant properties of Suaeda maritima (L.) Dumort

ethanolic extract on concanavalin-A induced hepatotoxicity in rats
S Ravikumar*, M Gnanadesigan, S Jacob Inbaneson & A Kalaiarasi
School of Marine Sciences, Department of Oceanography and Coastal Area Studies, Alagappa University, Thondi Campus,
Thondi 623 409, Tamil Nadu, India

Received 12 May 2010; Revised 16 March 2011

Hepatoprotective and antioxidant properties of Suaeda maritima (L.) Dumort on concanavalin-A induced stress in Wistar
albino rats have been reported. Rats were administered with ethanolic extract of Suaeda maritima at the concentration of 75,
150 and 300 mg/kg of body wt. for 9 days and concanavalin-A was administrated (iv) 12 mg/kg on 9th day. Rats in
concanavalin-A administered group showed elevated levels of AST, ALT, ALP and bilurubin. Pretreatment of rats with
ethanolic extract (300 mg/kg) significantly reduced these serum parameters compared to concavalin-A administered group.
Histopathological examination of liver sections showed that, normal liver architecture was disturbed by hepatotoxin
intoxication. The extract treated group and silymarin treated group retained the normal cell architecture, although less visible
changes were observed. Preliminary phytochemical analysis showed the presence of triterpenioids and may be responsible
for the hepatoprotective activity. The LD50 was calculated as 3 g/kg of the body weight. IC50 values of hydroxyl
(52.21±1.32µg/ml) and nitric oxide radicals (09.14±0.94 µg/ml) scavenging results showed comparable activity with
vitamin-C. Results of this study may be useful for the development of herbal medicine from Suaeda maritima for the
treatment of hepatitis.

Keywords: Acute toxicity, Concanavalin-A, Hepatoprotective, Salt marsh, Suaeda maritima

Suaeda maritima (L.) Dumort, belonging to
Chenopodiacea family is a salt marsh mangrove herb
similar to Suaeda monoica in appearance. The herb
prefers neutral and basic (alkaline) moist soils and can
grow in very alkaline and saline soils. Locally it is
called as umiri in Pichavaram and mattaumiri in
Muthupet, Tamil Nadu, India. The raw or cooked
young leave1 has a pleasant salty flavour and are often
mixed with other vegetables to reduce their saltiness.
The young shoots are pickled in vinegar and eaten on
their own or used as a relish. Traditionally, the leaf
from Suaeda maritima has been used as a medicine
for hepatitis2 and reported to have antiviral activity3-6
due to the presence of triterpenoids, sterols7,8. Modern
medicines have little to offer for alleviation of hepatic
disease and it is chiefly the plant based preparation
which is employed for the treatment of liver
disorders9. But there are not much drugs available for
the treatment of liver disorders10,11. It has been
reported that, several chemical constitutes of plant
——————
*
Correspondent author
Mobile : 0091-9443012752
Fax : 04561-243470
E-mail : ravibiotech201321@gmail.com
origin were evaluated for its possible hepatoprotective
activity against chemical induced liver damage in
experimental animals12-14. The present study was
aimed to evaluate hepatoprotective effect of ethanolic
extract of Suaeda maritima leaves using
concanavalin-A15 induced liver injury model in
Wistar rats.
Materials and Methods
Extraction—The fresh elder leaves of Suaeda
maritima were collected from Karangadu (Lat. 9° 38’
N and Lon. 78° 57’ E) mangrove forest, Ramnad
district, Tamil Nadu, India and their identity was
confirmed by following the standard monograph16.
The specimen sample was also authenticated by Prof.
K. Kathiresan, Centre of Advanced Study in Marine
Biology, Annamalai University, Porto Novo, Tamil
Nadu, India. The voucher specimen (AUOCAS002)
was also deposited at the School of Marine Sciences,
Department of Oceanography and Coastal Area
Studies, Alagappa University, Thondi Campus,
Thondi, India. The leaves were washed thrice with
distilled water to remove the contaminants and air
dried in shade. Coarsely powdered sample (500 g)
was defatted with petroleum ether (60-80ºC) and then
456 INDIAN J EXP BIOL, JUNE 2011
extracted with 1L of 95% (V/V) ethanol and water
mixture by percolation method. The extract was
concentrated under vacuum to the solvent free
residues. The percentage yield of extract was 52.64%
(w/w). Analysis of phytochemical constituents was
carried out by standard qualitative tests17.
In vitro antioxidant assay—Determination of
DPPH assay18, hydroxyl radical scavenging assay19,
nitric oxide radical scavenging assay20 and superoxide
radical scavenging assay21 were performed with
various concentrations (1.9 to 500 µg/ml) of S.
maritima leaf extract and various concentrations of
(1.9 to 500 µg/ml) vitamin C (positive control). The
IC50 values were calculated using linear regression
with Statplus pro 2009 software package.
Treatments—Male Wistar albino rats (150-200 g)
were maintained under standard conditions (23±2ºC,
relative humidity 55 ± 10% and 12:12 h LD cycle)
and allowed free accesses to food (Sai Durga Feeds
and Foods, Bangalore, India) and water. Experimental
protocols were approved by Institutional Animal
Ethics Committee, Alagappa University, Tamil Nadu,
India.
For the determination of median lethal dose (LD50)
animals (9) were kept fasting for overnight providing
only water, after which the extracts were
administrated orally at different doses of 250-5000
mg/kg and all the rats were observed for the physical
signs of toxicity for 14 days. If the mortality was
observed in 6 out of 9 animals, then the dose
administrated was assigned as toxic dose. If mortality
was observed in 3 animals, then the same dose
was repeated again to confirm the toxic dose. One
tenth of the maximum dose of the extract tested
for acute toxicity was selected for evaluation
of hepatoprotective activity22 through following
treatments.
The animals were divided into 6 groups consisting
of 6 per group.
Group I (vehicle control) animals were treated with
distilled water (5 ml/kg body wt) for 9 days and kept
as control group.
Group II (hepatotoxin group) animas were treated
with distilled water (5 ml/kg body wt) for 9 days +
single dose of (12 mg/kg body wt, iv) concanavalin-A
on 9th day with liquid paraffin (1:1) and hepatotoxin
group.
Group III treated with silymarin23 at the dose of
100 mg/kg body wt, was administrated through oral
gavage for 9 days + single dose of (12 mg/kg body
wt, iv) concanavalin-A on 9th day with liquid paraffin
(1:1) and kept as positive control group.
Animals of group IV, V and VI were treated with
ethanolic extracts of 75, 150 and 300 mg/kg body wt.
were administrated through oral gavage for 9 days +
single dose of (12 mg/kg body wt., iv) concanavalin-
A on 9th day with liquid paraffin (1:1) and kept as
treatment groups.
Analysis of clinical parameters—On the 10th day
all the animals were anesthetized with ether. Blood
samples were collected from jugular vein. The blood
samples were allowed to clot for 45 min at room
temperature. Serum was separated by centrifugation at
600 × g for 15 min and analyzed for AST, ALT, ALP
and bilurubin. Blood standard commercial kit (CML-
Biotech PVT. Ltd, India) were used to measure the
level of AST, ALT, ALP and Bilurubin. All the
determinations were carried out by an auto analyzer
of Merck make (300TX, E-Merck-Micro Labs,
Mumbai). The hepatoprotective activity (% H), was
calculated as follows:
(T − V )
1− × 100
(C − V )
Where T is mean value of drug and concanavalin-
A, C mean value of concanavalin-A alone and V is
the mean value of normal control animals. Values are
expressed as mean ± SD which for biochemical
parameters statistically using one way ANOVA for
comparison with control group and concanavalin-A
treated group. P<0.05 was considered as significant.
Histopathological studies—For the histopathological
study, the liver of 6 animals from each group were
immediately removed after autopsy and the tissues
were fixed in bouin’s solution for 12 h, then
embedded in paraffin using conventional methods24
and cut in to 5 µm thick sections and stained using
haematoxylin-eosin dye and finally mounted in
diphenyl xylene. The sections were observed under
microscope for histopathological changes. Histological
damage was expressed using the following score
system: ∅ absent; ⊥ few; + mild; ++ moderate; +++
severe; ++++ extremely severe (the liver of 6 animals
in every group were examined with 10 different
microscopic fields).
Results and Discussion
In Indian system of medicine, certain herbs are
claimed to provide relief against liver disorders. The
 RAVIKUMAR et al.: HEPATOPROTECTIVE & ANTIOXIDANT EFFECT OF SUAEDA MARITIMA 457

claimed therapeutic reputation has to be verified in a aspartate and amino transferase enzymes were
scientific manner. In the present study one such maintained at near normal level in the oral
extract of Suaeda maritima was taken for the administrated group of plant extract as compared with
hepatoprotective study. Preliminary phytochemical the hepatotoxin group. Alkaline phosphatase activity
screening of the ethanolic extract of the leaf Suaeda on endothelial cell surface is responsible for the
maritima showed the presence of reducing sugars, conversion of adenosine nucleotide to adenosine, a
steroids, and triterpenes. In the toxicity study, no potent vasodilator and anti inflammatory mediator
mortality occurred throughout the experiment with the that results from injury. So, following, accumulation
doses of plant extract and silymarin treated group. of IL-6 can leads to the production of adenosine to
The ethanolic extract did not show any mortality up to alkaline phosphatase, this may be the reason for the
the level of 3000 mg/kg and were considered as safe. increment in ALP in hepatotoxin group. Bilurubin is a
Single dose of concanavalin-A is sufficient for the major breakdown product that results from the
development of liver lesions. Concanavalin-A destruction of RBC which is removed from the blood
induced hepatitis is both T-cell and macrophage by the liver through conjugation and secreted into bile
dependent. The precise mechanism(s) by which usually becomes elevated as a result of decreased
T-cells and macrophages exert their hepatogenic uptake by the liver, decreased conjugation, decrease
secretion from the liver or blockage of the bile ducts
potential is not known. Because a massive release of
that is caused in liver damage36. The oral
macrophage and T-cell derived cytokines IL-2, IL-1,
administration of plant extract and (positive drug)
IL-6, tumor necrosis factor-alpha (TNF-α), interferon-
gamma (IFN-γ) and granulocyte macrophage colony
stimulating factor (GM-CSF) occurs with different
kinetics in response to concanavalin-A, a role has
been envisaged for these cytokines in the
development of the hepatic lesions25. It is evident that,
the concanavalin-A produced liver inflammation due
to the severe hepatic necrosis. It is know that an
increasing the enzymatic activity of ALP and AST in
the serum directly reflects the major permeability of
cell membrance26-28. An increase in AST and ALT, a
hepatospecific enzyme that is principally found in the Fig.1—Effect of ethanolic extract of Suaeda maritima and
silymarin (Positive control) on serum level of AST, ALT and ALP
cytoplasm in rats29 following the administration of (IU/L) during concanavalin-A induced hepatotoxin rats. [Values
CCl4 is attributed to the increased release of the are mean ± S.D. (n=6). aGroup II (concanavalin-A treated rats)
enzymes from damaged liver parenchymal cells30-33. compared with group I (control rats). bGroup III, IV, V and VI
Similar results of ACP and ALP were found to (silymarin and plant extract treated rats) compared with Group II
increase in hepatotoxin animals34,35. (concanavalin-A treated rats), CP<0.05].
In the present study concanavalin-A administrated
group showed significantly increased levels of AST,
ALT, ALP (Fig.1), direct and indirect bilurubin
(Fig. 2). Amino transferase is an important class of
enzymes linking carbohydrate and amino acid
metabolism there by clearly establishing the
relationship between the intermediates of the citric
acid and amino acids. Alanine amino transferase and
aspartate amino transferase are well known diagnostic
indicators of liver diseases. In case of liver damage
with hepatocellular lesions and parenchymal cell Fig.2 —Effect of ethanolic extract of Suaeda maritima and
necrosis, these enzymes are released from the silymarin (Positive control) on serum level of total and direct
damaged tissue into the blood stream. The decrease in bilurubin (mg/dl) during concanavalin-A induced hepatotoxin
rats. [Values are mean ± S.D. (n=6). aGroup II (concanavalin-A
alanine amino transferase activity is usually treated rats) compared with group I (control rats). bGroup III, IV,
accompanied by lowering in the activity of aspartate V and VI (silymarin and plant extract treated rats) compared with
amino transferase, in the present study the activities of Group II (concanavalin-A treated rats), CP<0.05].
458 INDIAN J EXP BIOL, JUNE 2011

silymarin 100 mg/kg were significantly reduced the of plant extract and vitamin C were represented in
level of marker enzymes. The hepatoprotective Table 3. It revealed that, hydroxyl radical scavenging
activity of different doses was also observed and (52.21 ± 1.32 µg/ml) and nitric oxide scavenging
maximum activity of 80.90% was noticed with (09.14 ± 0.94 µg/ml) activity showed comparable
300 mg/kg of the plant extract (Table 1). activity with the standard vitamin C (44.24 ± 1.50 µg/ml
Histopathological scores (Table 2) showing the and 4.98 ± 1.28 µg/ml). Previously, it was reported
severity level of fatty changes and hydrophic changes that, reactive oxygen species play a major role in
in concanavalin-A treated rats but, mild level of fatty Concanavalin-A induced hepatitis through secondary
changes were observed with silymarin and extract immune mediated liver damage37 and the
(300 mg/kg) treated rats, moreover focal necrosis hepatoprotective effect of S. maritima leaf extract
were observed with severe level in concanavalin-A might be due to the presence of antioxidant
treated rats but few level of necrosis were observed properties18.
with extract and silymarin treated rats.
It is concluded that, administration of
Histopathological examination of liver sections of
concanavalin-A resulted in a significant increase in
control group showed normal cellular architecture
the AST, ALP, ALT and bilurubin level and these
with distinct hepatic cells, sinusoids space and proper
changes in the marker levels reflected in hepatic
central vein (Fig. 3). Whereas concanavalin-A
structural integrity. Pretreatment with alcoholic
induced rats showed distorted sinusoids and hepatic
extract of Suaeda maritima attenuated the elevated
necrosis (Fig. 3b). Rats pretreated with silymarin (100
level of serum markers. Normalization of serum
mg/kg) and ethanolic extract (300 mg/kg) followed by
markers by ethanolic extracts suggested that,
concanavalin-A hepatotoxicity showed a sign of
hepatocytes are conditioned to protect the membrane
protection as it was evident from the reduction of
integrity against concanavalin-A induced leakage of
necrosis and normalization of sinusoidal structure
marker enzymes into the circulation. Elevated level of
(Figs 3c-f).
bilurubin indicates the hepatotoxicity. The
Results of DPPH assay, hydroxyl radical normalization of the blood bilurubin extract in pre-
scavenging activity, nitric oxide radical scavenging treated rats further indicated the protective nature of
activity and superoxide radical scavenging assay the extract on hepatic cells. Histopathological
Table 1––Effect of Suaeda maritima on hepatoprotection on examination of liver sections revealed that, the normal
concanavalin-A induced hepatotoxicity liver architecture was disturbed by hepatotoxin
Hepatoprotection
intoxication. Sections obtained from the plant extract
Dose
Treatments and silymarin groups showed normal cell architecture,
(mg/kg) (%)
although less visible changes were observed which
Vehicle control Nil Nil
further corroborate the hepatoprotective activity. The
Con-A treated Nil Nil
Con-A+ Silymarin 100 61.38
hepatoprotective activity of Suaeda maritima may be
Con-A+Extract (75 mg/kg) 75 26.52 due to the presence of triterpene phyto-chemical
Con-A+Extract (150 mg/kg) 150 52.0 constituents. Hence, triterpenes are proved to have
Con-A+Extract (300 mg/kg) 300 80.90 hepatoprotective activity38. Further studies are
Table 2––Histopathological changes in the liver of the rats treated with silymarin and plant extract

Microscopicobservation
Treatments Degeneration in Deformation in Focal Congestion in Congestion in Bleeding area in
hepatocytes (fatty and hepatocytes necrosis central vein sinusoids hepatic lobes
hydrophic changes)
Vehicle control + ∅ ∅ + ∅ ∅
Con-A treated ++++ +++ +++ ++ ++ ++
Con-A + Silymarin + ⊥ ⊥ + ⊥ ⊥
Con-A + Extract 75 mg/kg +++ ++ ++ ++ ++ +
Con-A + Extract 150 mg/kg ++ + ⊥ + + +
Con-A + Extract 300 mg/kg + ⊥ ⊥ ++ + ⊥
∅ absent: ⊥ few: + mild: ++ moderate: +++ severe: ++++ extremely severe (the liver of 6 animals in every group were examined)
 RAVIKUMAR et al.: HEPATOPROTECTIVE & ANTIOXIDANT EFFECT OF SUAEDA MARITIMA 459

Fig. 3—(a) Liver section of control rat showing normal cellular architecture with distinct hepatic cells, sinusoidal spaces and portal vein;
(b) Liver section of concanavalin-A rat showing disarragment and regrrangmetn of vaculed hepatic cells and hepatic necrosis; (c) Liver
section of silymarin treated rat showing less fatty change formation and reductioin in hepatic necrosis; (d) Liver section of the rat treated
with Plant extract 75 mg/kg and concanavalin-A, 100 ×, heamatoxilin-eosin stain. Liver section of the rat shows fatty change formation
and hepatic necrosis; (e) Liver section of the rat treated with plant extract 150 mg/kg and concanavalin-A, 100 ×, haematoxilin and eosin
stain. Liver section of the rat showing reduction in fatty change formation and hepatic necrosis.; (f) Liver section of the rat treated with
plant extract 300 mg/kg and concanavalin-A, 100 ×, haematoxilin and eosin stain. Liver section of the rat showing normal architecture
with less fatty change formation and reduction in hepatic necrosis. H & E 100 × [CV: Central Vein; S: Sinusoidal spaces; H: Hepatocytes;
F: Fatty changes; N: Hepatic necrosis].
3 Padmakumar K & Ayyakkannu K, Antiviral activity of
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