J Basic Clin Physiol Pharmacol 2015; 26(1): 95–103

Vijayasteltar B. Liju, Kottarapat Jeena and Ramadasan Kuttan*

Gastroprotective activity of essential oils from

turmeric and ginger
Abstract Introduction
Background: Turmeric (Curcuma longa) and ginger (Zingiber
Essential oils from spices are gaining greater interest as
officianale) are widely used in Asian countries as traditional
natural antioxidants, food preservatives and additives.
medicine and food ingredients. In the present study, we have
Essential oil contains a number of chemical constituents,
evaluated the gastroprotective activity of turmeric essential
and this complex combination of compounds gives its
oil (TEO) and ginger essential oil (GEO) in rats.
characteristic fragrance and flavor. The use of essential
Methods: Turmeric and ginger were evaluated for their
oils is increasing rapidly in most of the countries in food
antiulcer activity against ethanol-induced ulcers in male
industries, production of soaps, detergents, cosmetics,
Wistar rats at different doses: 100, 500 and 1000 mg/kg
nonalcoholic beverages, oral care products, aromather-
body weight. Ethanol was used to induce gastric ulcer in
apy and pharmacology [1]. Their potential anticancer pre-
Wistar rats. Parameters such as ulcer index, histopathol-
vention and treatment activities have been investigated in
ogy and levels of antioxidant enzymes such as glutathione
recent years [2]. Turmeric essential oil (TEO) and ginger
peroxidase (GPx), superoxide dismutase (SOD), catalase
essential oil (GEO) have been reported to have several bio-
and glutathione (GSH) levels were measured to assess the
logical properties such as antioxidant, anti-inflammatory
degree of protection produced by the essential oils.
and antinociceptive activities [3, 4]. TEO showed neuro-
Results: TEO and GEO inhibited ulcer by 84.7% and
protective effect against cerebral ischemia and attenua-
85.1%, respectively, as seen from the ulcer index. Reduced
tion of delayed neuronal death via a caspase-dependent
antioxidant enzymes such as GPx, SOD, catalase and GSH
pathway as well as significantly reduced nitrosative stress
produced by alcohol administration were significantly
[5, 6]. The chemopreventive efficacy of TEO against sub-
(p < 0.001) increased by simultaneous administration of
mucous fibrosis in humans has been reported [7]. TEO has
TEO and GEO. Histopathological examination showed
antimutagenic and anticancer properties [8, 9]. Antimi-
that ethanol-induced lesions such as necrosis, erosion
crobial, anticancer, immunomodulatory and antiarthritic
and hemorrhage of the stomach wall were significantly
properties of GEO have been reported [4, 10, 11]. GEO has
reduced after oral administration of essential oils.
also shown the ability to suppress the formation of DNA
Conclusions: Results suggest that TEO and GEO could
adducts [12]. The Food and Drug Administration approved
reduce the gastric ulcer in rat stomach as seen from the
TEO and GEO as food additives and these are listed
ulcer index and histopathology of the stomach. Moreover,
as Generally Recognized as Safe (GRAS). Reports also
oxidative stress produced by ethanol was found to be sig-
showed that oral administration of TEO and GEO have no
nificantly reduced by TEO and GEO.
subchronic and genotoxicity in rats [13, 14].
Peptic ulcers are currently considered as a global
Keywords: antioxidant; antiulcer; ginger essential oil; his-
health problem affecting thousands of people. About
topathology; turmeric essential oil.
300,000 people in the world die each year from com-
DOI 10.1515/jbcpp-2013-0165
plications of peptic ulcer diseases. Studies from differ-
Received December 20, 2013; accepted March 5, 2014; previously ent parts of India propose its incidence to be 4–10 per
published online April 21, 2014 thousand population, and some of the states are consid-
ered to be very high-risk areas. The estimated lifetime
*Corresponding author: Dr. Ramadasan Kuttan, PhD, Research occurrence of gastric ulcer is 12% for men and 9% for
Director, Amala Cancer Research Centre, Amala Nagar, Thrissur, women [15]. The etiology of ulcer is not clear, but it is
Kerala-680 555, India, Phone: +91-487-2307968,
generally accepted that it results from an imbalance
Fax: +91-487-2307968, E-mail: amalacancerresearch@gmail.com;
amalaresearch@hotmail.com
between some gastroprotective (mucus-bicarbonate
Vijayasteltar B. Liju and Kottarapat Jeena: Department of Biochemistry, secretion and prostaglandins) and aggressive factors
Amala Cancer Research Centre, Amala Nagar, Kerala, India (acid, pepsin, Helicobacter pylori and bile salts) [16, 17].

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96      Liju et al.: Gastroprotective effect of essential oils
Stress, smoking, nutritional deficiencies and ingestion
of nonsteroidal anti-inflammatory drugs are factors
that increase the incidence of gastric ulcer [18]. Studies
have shown that reactive oxygen species, especially the
hydroxyl radical, lipid peroxidation, various chemical
agents, food ingredients and drugs have an important
role in the destruction of mucosal integrity and delaying
the healing of gastric ulcers. Ethanol-induced gastric
lesion is complex, and the mechanisms underlying the
development of gastric lesions by ethanol are consid-
ered to be due to depletion of non-protein sulfhydryl
concentration, modulation of the nitric oxide system
and reduction of gastric mucosal blood flow [19]. Oxida-
tive stress and depletion of antioxidants are also critical
strides in alcohol-induced mucosal damage. The causes
of ulceration in the experimental models are varied.
Alcohol-induced lesions of gastric mucosa are thought
to arise as a result of direct damage of gastric mucosal
cells, resulting in the development of free radicals that
support the aggressive factors, whereas weakness of the
protective factors lead to gastric ulcer.
In this study, using an ethanol-induced ulcer model
in rats, we have evaluated the antiulcer potential of the
essential oils isolated from turmeric (Curcuma longa L.)
and ginger (Zingiber officinale Roscoe) belonging to the
family Zingiberaceae.
Materials and methods
Essential oils
Turmeric and ginger were cultivated locally and the essential oils were
isolated by steam distillation from the rhizome of turmeric and ginger.
They were purchased from Kancore Ingredients Limited, Angamali,
Kerala, India. The color and appearance of TEO was pale yellow liquid
(sample no. TONE-00321). GEO (sample no.GIO-91204) was supplied
as a pale yellow to light amber-colored liquid. The essential oils were
stored at 4 °C away from direct light and heat. The essential oils were
dissolved in paraffin oil for in vivo antiulcer studies. Gas chromatogra-
phy-mass spectrometry (GC/MS) analysis showed that TEO contained 13
compounds of which ar-turmerone (61.79%), curlone (12.48%) and ar-
curcumene (6.11%) were found to be most prominent [3]. Out of the 18
compounds of GEO analyzed by GC/MS, α-zingiberene (31.08%) was the
major constituent, and some other compounds such as ar-curcumene
(15.35%), β-sesquiphellandrene (14.02%), β-bisabolene (13.81%), sabi-
nene (8.28%) and camphene (5.14%) were also identified [4].
Chemicals and reagents
Nitroblue tetrazolium (NBT), glutathione (GSH), glutathione oxi-
dized (GSSG), nicotinamide adenine dinucleotide phosphate
reduced (NADPH) and 5,5′-dithiobis 2-niotrobenzoic acid (DTNB)
were purchased from Sisco Research Laboratories Pvt. Ltd., Mumbai,
India. Liquid paraffin (CAS no. 8012-95-1) was purchased from Merck
Specialties Private Ltd., Mumbai, India. All other chemicals and
­reagents used were of analytical reagent grade.
Animals
Wistar rats (150–200 g) were purchased from Small Animal Breed-
ing Station, Mannuthy, Kerala, India and housed in well-ventilated
cages under controlled conditions of light and humidity and pro-
vided with normal mouse chow (Sai Durga Food and Feeds, Banga-
lore, India) and water ad libitum. All the animal experiments were
done according to the instructions prescribed by the Committee for
the Purpose of Control and Supervision of Experiments on Animals
(CPCSEA), Ministry of Environment and Forest, Government of India,
and implemented through the Institutional Animal Ethical Commit-
tee (Sanction No. 149/1999/CPCSEA).
Alcohol-induced gastric ulcer
Nine groups of male Wistar rats, with each group consisting of five
animals were used for this study (Table 1). Different doses of TEO
and GEO at the concentrations of 100, 500 and 1000 mg/kg body
weight were given for seven consecutive days by oral gavage prior to
the experiment. All the rats were kept for 24 h without any food and
devoid of both water and food for 12 h prior to ethanol administra-
tion. One hour after the last drug treatment, all the rats in groups
II–IX were treated with absolute alcohol (5 mL/kg body weight) orally
to induce ulceration [20]. All animals were sacrificed after 3 h. After
alcohol administration, the stomach was excised and washed with
ice-cold saline, and ulcer index (UI), histopathology and antioxidant
enzyme evaluation was done.
Estimation of UI
The UI was calculated to find out the severity of gastric mucosal
lesions, which is graded as erosions [21]. Lesions less than 1 mm are
scored as grade I, 1–2 mm are scored as grade II and more than 2 mm
are scored as grade III. The UI was calculated by the formula:
Table 1 The nine groups of male Wistar rats, each group consisting
of five animals.
Group  Treatment
I   Untreated
II   Absolute ethanol (5 mL/kg b.wt.)
III   Absolute ethanol (5 mL/kg b.wt.)+paraffin oil
IV   Absolute ethanol (5 mL/kg b.wt.)+TEO 100 mg/kg b.wt.
V   Absolute ethanol (5 mL/kg b.wt.)+TEO 500 mg/kg b.wt.
VI   Absolute ethanol (5 mL/kg b.wt.)+TEO 1000 mg/kg b.wt.
VII   Absolute ethanol (5 mL/kg b.wt.)+GEO 100 mg/kg b.wt.
VIII   Absolute ethanol (5 mL/kg b.wt.)+GEO 500 mg/kg b.wt.
IX   Absolute ethanol (5 mL/kg b.wt.)+GEO 1000 mg/kg b.wt.
b.wt., body weight.
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1×(number of lesions in grade I) + 2×(number of lesions in grade II)+3 ×(number of lesions in grade III)
UI =
10
Percentage protection was calculated from the following for-
mula: [(UI control–UI treated)/UI control] × 100. Photographs of the
excised stomach were recorded.
Effect of essential oils antioxidant enzymes
activity in gastric mucosa
The mucosa of glandular stomach from the rats in all groups was
removed and 10% homogenate was prepared in Tris buffer (0.1 M,
pH 7.4). The total protein was estimated by the method of Lowry et al.
[22]. GSH, glutathione peroxidase (GPx), catalase and superoxide dis-
mutase (SOD) were estimated in the mucosa of glandular stomach by
the following methods.
Glutathione
GSH was measured by its reaction with DTNB, which produced a yellow-
colored complex with absorption maximum at 412 nm. Sample (100 μL)
was mixed with 25% trichloroacetic acid (TCA) (125 μL) and cooled in ice
for 5 min. The mixture was further diluted with 0.6 mL of 5% TCA and
centrifuged for 5 min; the resulting supernatant was taken for GSH esti-
mation. The volume of the aliquot was made up to 1 mL with 0.2 M phos-
phate buffer (pH 8). Two milliliters of freshly prepared 0.6 mM DTNB was
added to the tubes and the intensity of the yellow color was measured at
412 nm. Values are expressed as nanomoles per milligram protein [23].
Glutathione peroxidase
GPx degrades hydrogen peroxide in the presence of GSH, thereby
depleting it. The remaining GSH is measured using DTNB, which
gives a colored complex. Reaction mixture (2.5 mL) containing 2 mM
GSH, 0.4 mM phosphate buffer (pH 7), 1 mM NaN3, sample (100 μL)
and 0.25 mM H2O2 was incubated and the reaction was stopped by the
addition of 2 mL of 1.67% H2PO3. After centrifugation, 2 mL of super-
natant was added to the mixture of 0.4 M Na2HPO4 and 1 mM DTNB.
After 10  min of incubation, the absorbance of the reaction mixture
was measured at 412 nm. One unit of enzyme activity was defined as
a decrease in log GSH by 0.001/min after a subtraction of the decrease
in log GSH/min for the nonenzymatic reaction and expressed as units
of enzyme acting per milligram protein [17].
Catalase
Catalase activity was estimated by the method of Aebi [24]. The
disintegration of hydrogen peroxide by catalase enzyme and its
absorbance was measured at 240 nm for 3 min at 1-min intervals. The
reaction mixture contained 1.9 mL of 0.5 M phosphate buffer (pH 7),
1 mL of H2O2 and 0.1 mL of sample. Control sample was placed in the
Liju et al.: Gastroprotective effect of essential oils      97
reference containing 0.1 mL of sample and 2.9 mL of buffer. Catalase
activity was calculated using the molar extinction coefficient of 43.6.
Values are expressed as nanomoles of H2O2 consumed per minute per
milligram of protein sample.
Superoxide dismutase
SOD activity was determined by the method of McCord and Fridovich
[25]. The activity was based on the ability of the enzyme to inhibit the
reduction of NBT by superoxide (O2–), which is generated by the reac-
tion of photoreduced riboflavin with O2. Based on the reaction, NBT is
reduced to a formazan blue. Total 2.95-mL reaction mixture contained
sample, 200 μL of (0.1 M) EDTA, 0.0015% NaCN, 100 μL of NBT (0.15 mM)
and phosphate buffer (67 mM, pH 7.8). After the addition of 0.05 mL of
riboflavin, the absorbance of the solution was measured against dis-
tilled water at 560 nm. This mixture was then uniformly illuminated
with an incandescent lamp for 15 min and the absorbance was taken
again at 560 nm. Values are expressed as units per milligram protein.
Histopathological analysis
A portion of the stomach was cut, washed in phosphate-buffered
saline and fixed in 10% neutral buffered formalin. Sections (4 μm)
were taken and stained with hematoxylin-eosin and examined under
the microscope (40 × ) for histopathological changes such as conges-
tion, hemorrhage, erosion and necrosis.
Statistical analysis
Values were expressed as mean ± SD. The statistical significance was
compared between control and experimental groups by one-way
analysis of variance (ANOVA) followed by the appropriate post hoc
test (Dunnett multiple comparison test) using GraphPad software
(version 3.05, La Jolla, CA, USA). Data of essential oil-treated animals
were compared with that of control animals.
Results
Effect of essential oils on the morphology of
stomach treated with absolute alcohol
The morphology of normal (untreated) stomach did not
show any lesions and bleeding. Administration of abso-
lute ethanol resulted in severe gastric damage visible from
the outside of the stomach as thick dark reddish lines and
the UI was found to be 4.77 ± 0.56 (Figure 1). Pretreatment
of rats with the highest dose (1000 mg/kg body weight)
of TEO reduced the UI to 0.73 ± 0.21 (p < 0.001) (Table 2).
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98      Liju et al.: Gastroprotective effect of essential oils

A B

C D

Figure 1 Effect of TEO and GEO on the morphology of rat stomach in gastric ulcers induced by absolute alcohol.
(A) Untreated stomach. (B) Treated with absolute alcohol alone (5 mL/kg body weight). (C) Treated with absolute alcohol and paraffin oil.
(D) Treated with absolute alcohol and TEO (1000 mg/kg body weight). (E) Treated with absolute alcohol and GEO (1000 mg/kg body weight).

Table 2 Effect of TEO and GEO on gastric damage produced by ethanol administration.

Groups   UI   Percentage inhibition, %

Untreated   Nil  
Control (absolute ethanol alone)   4.77 ± 0.56  
Vehicle control (paraffin oil+absolute ethanol)   4.22 ± 0.39  
TEO 100 mg/kg body weight+absolute ethanol   1.68 ± 0.47a   64.8
TEO 500 mg/kg body weight+absolute ethanol   1.43 ± 0.64a   70.0
TEO 1000 mg/kg body weight+absolute ethanol   0.73 ± 0.21a   84.7
GEO 100 mg/kg body weight+absolute ethanol   1.88 ± 0.58a   60.6
GEO 500 mg/kg body weight+absolute ethanol   1.47 ± 0.78a   69.2
GEO 1000 mg/kg body weight+absolute ethanol  0.71 ± 0.28a   85.1

Each value represents the mean ± SD of six rats. ap < 0.001 when compared with control. UI, ulcer index.

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Similarly, the animals treated with 500 and 100 mg/kg
body weight TEO showed protection against the ulcerating
effect of ethanol in a concentration-dependent manner, as
evidenced by the UI of 1.43 ± 0.64 (p < 0.001) and 1.68 ± 0.47
(p < 0.001), respectively. The UI values were 0.71 ± 0.28
(p < 0.001), 1.47 ± 0.28 (p < 0.001) and 1.88 ± 0.58 (p < 0.001)
for the groups treated with 1000, 500 and 100 mg/kg body
weight of GEO, respectively (Table 1).
Effect of essential oils on in vivo antioxidant
enzymes in the gastric mucosa after ethanol
treatment
Glutathione
Ethanol administration decreased the gastric mucosal
level of GSH. GSH level was found to be significantly
increased in 500 and 1000 mg/kg body weight TEO- and
GEO-treated groups (p < 0.01) in a concentration-depend-
ent manner (Figures 2 and 3) when compared with the
control group.
Catalase activity
Compared to normal rats, there was a decrease in catalase
level in the alcohol-treated group. Catalase was found to
be significantly increased (p < 0.001) in rats treated with
TEO and GEO when compared with the control group
(Figures 2 and 3).
SOD activity
The level of SOD in stomach tissue was found to be
decreased by ethanol administration when compared to
the normal levels. TEO- and GEO-treated groups showed
significant elevation (p < 0.001) of SOD level in stomach
mucosa of treated groups (Figures 2 and 3).
GPx activity
GPx level in gastric mucosa was found to be lowered fol-
lowing absolute alcohol administration (Figures 2 and 3).
The level of GPx enzyme was found to be increased by
administration of TEO and GEO at 1000 (p < 0.01), 500
(p < 0.01) and 100 (p < 0.05) mg/kg body weight in a con-
centration-dependent manner.
Liju et al.: Gastroprotective effect of essential oils      99
Histopathological analysis
Absolute alcohol-treated stomach revealed histopatho-
logical lesions including necrosis and inflammatory
exudates. Mucosa, submucosa and muscularis mucosa
showed diffuse infiltration by lymphocytes and plasma
cells. Pretreatment with 1000 mg/kg body weight TEO
and GEO restored the tissue integrity and structure as
well as mucosa, submucosa, muscularis mucosa, muscle
layer and serosal layer, which showed normal appearance
(Figure 4).
Discussion
Ethanol represents one of the most common causes of
gastric ulcer in humans [26]. Ethanol-induced gastric
ulcer models in rats have been widely used for the evalu-
ation of gastroprotective activity. Ethanol induces intense
gastric ulcers as it promotes the disturbances in the gastric
mucosa [27], leading to the formation of characteristic
necrotic and hemorrhagic lesions due to a reduction in
the gastric blood flow, mucus production and bicarbonate
secretion [28]. The metabolism of ethanol with alcohol
dehydrogenase produces acetaldehyde, a highly reactive
toxic by-product that may contribute to tissue damage and
ulcer. TEO and GEO were found to significantly inhibit
ulcers at all doses tested in a dose-dependent manner. It
is evident from this study that administration of essential
oils maintained the integrity and structure of the gastric
mucosa as shown by reduced UI when compared to the
control group.
Development of these ulcers, which is predominant in
the glandular part of the stomach, is reported to stimu-
late the formation of reactive oxygen species, especially
hydroxyl radicals [29], resulting in the damage to rat
gastric mucosa. Ethanol-induced generation of free radi-
cals elevates the lipid peroxide level and increases malon-
dialdehyde, gastric vascular permeability, histamine
release and production of leukotrienes, thereby depleting
GSH levels, prostaglandin synthesis in gastric mucosa
and induces macroscopic mucosal ulceration. Ethanol-
induced ulcer also stimulates the formation of leukotriene
C4 (LTC4) and mast cell secretory products [30].
Antioxidants play an appreciable role in healing
these ulcers by restoring the altered gastric protective
factors [27]. Metabolism of alcohol involves cytochrome
P450 enzyme (CYP2E1), which oxidizes alcohol to acet-
aldehyde, which produces significant damage to the
stomach lining [31]. Our previous study indicated that
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100      Liju et al.: Gastroprotective effect of essential oils

A 7 B 45
***
6 40 ***
5 * ** 35
**
U/mg protein

U/mg protein
30
4 25 *
3 20
2 15
10
1 5
0 0
Untreated Control Paraffin oil TEO 100 TEO 500 TEO 1000 Untreated Control Paraffin oil TEO 100 TEO 500 TEO 1000
mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg
Catalase Glutathione peroxidase

C D 3.5
30
***
** 3.0
25 **
***
nmol/mg protein

* 2.5

U/mg protein
20 ***
2.0
15
1.5
10 1.0
5 0.5
0 0
Untreated Control Paraffin oil TEO 100 TEO 500 TEO 1000 Untreated Control Paraffin oil TEO 100 TEO 500 TEO 1000
mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg
Glutathione Superoxide dismutase

Figure 2 Effect of TEO on gastric mucosal antioxidant enzymes and GSH in alcohol-induced gastric ulcer in rats.
(A) Catalase. (B) GPx. (C) GSH. (D) SOD. Values are mean ± SD from six animals in each group; *p < 0.05, **p < 0.01, ***p < 0.001. Significance
was calculated for the comparison of treated groups with the control group.

A 7 B 45
6 ** 40
* **
** 35
5 **
U/mg protein

U/mg protein

30 *
4 25
3 20
2 15
10
1 5
0 0
Untreated Control Paraffin oil GEO 100 GEO 500 GEO 1000 Untreated Control Paraffin oil GEO 100 GEO 500 GEO 1000
mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg

C 30 D 3.0
** ** ***
25 2.5 ***
**
nmol/mg protein

U/mg protein

20 2.0 ***
15 1.5
10 1.0
5 0.5
0 0
Untreated Control Paraffin oil GEO 100 GEO 500 GEO 1000 Untreated Control Paraffin oil GEO 100 GEO 500 GEO 1000
mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg

Figure 3 Effect of GEO on gastric mucosal antioxidant enzymes and GSH in alcohol-induced gastric ulcer in rats.
(A) Catalase. (B) GPx. (C) GSH. (D) SOD. Values are mean ± SD from six animals in each group; *p < 0.05, **p < 0.01, ***p < 0.001. Significance
was calculated for the comparison of treated groups with the control group.

TEO and GEO can significantly inhibit the cytochrome assessing the efficacy of antiulcer drugs. These markers,
P450 enzymes especially CYP2E1 in vitro and in vivo [32]. which were significantly lowered in the gastric mucosa
Biochemical analysis of gastric mucosa for antioxidants of ethanol-treated animals, were found to be markedly
such as catalase, GPx, SOD and GSH are highly useful in increased by administration of essential oils. These

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 Liju et al.: Gastroprotective effect of essential oils      101

A B

C D

Figure 4 Histological evidence for the protective effect of TEO and GEO on ethanol-induced gastric damage in rats (hematoxylin and eosin
staining).
(A) Stomach wall of untreated rat showing its normal appearance. (B) Stomach wall of rat after treatment with absolute alcohol. (C) Stomach
wall of rat treated with absolute alcohol and paraffin oil. (D) Stomach wall of rat treated with TEO (1000 mg/kg body weight) and absolute
alcohol. (E) Stomach wall of rat treated with GEO (1000 mg/kg body weight) and absolute alcohol.

results indicate that the mechanism of action of TEO
and GEO involves their potential to act as antioxidants
through the stimulation of antioxidant enzymes such
as GPx, SOD and catalase as well as GSH and its inhibi-
tion of CYP2E1, which oxidizes alcohol to reactive oxygen
species [3, 4, 32].
Free radicals play a major role in gastric ulcer [33].
The role of GSH is defense against dietary xenobiotics
and lipid peroxidation [34]. Depletion of gastric mucosal
GSH may result in the accumulation of free radicals
and leads to membrane damage by lipid peroxidation.
Ethanol administration decreased the gastric mucosal
level of GSH. GSH is important for the maintenance of
mucosal integrity. Ethanol-induced generation of free
radicals elevates the lipid peroxide level and reduces
cysteine, which is required for GSH synthesis, thereby
depleting GSH levels [35]. The decrease in catalase levels
leads to an increase in the accumulation of reactive
oxygen species (ROS), which can elevate the intensity
of lipid peroxidation, tissue damage and increased per-
oxidase activity. In this study, SOD activity was signifi-
cantly decreased due to excess production of superoxide
anion by ethanol administration. This enzyme is one of
the cellular defenses against oxidative damage, and it is
an important enzyme that catalyzes the dismutation of
superoxide anions into O2 and H2O2 [36]. GPx is selenoen-
zyme that protects the lipid membranes and other cellu-
lar components against oxidative damage. GPx catalyzes

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102      Liju et al.: Gastroprotective effect of essential oils
the reduction of H2O2 and hydroperoxides to nontoxic
products with the help of GSH. The bioavailability of
essential oil might be playing an important role in the
therapeutic effect. TEO bioavailability study showed that
the blood plasma levels of ar-turmerone and curlone
were maintained at the range of 100–135 and 8–16 ng/
mL, respectively, from 8 to 18 h. Blood serum analysis
after oral administration of GEO in rats exhibited the
presence of zingiberene at 2 h. Thus, TEO as well as GEO
showed prolonged systemic availability and bioavail-
ability [14, 37].
Previous studies in our laboratory have recognized
that TEO and GEO are nontoxic and nonmutagenic to
animals and they act as strong antioxidants and anti-
inflammatory and antinociceptive agents [3, 4, 13, 14].
The major constituent of TEO is ar-turmerone (61.79%),
whereas that of GEO is zingiberene (31.08%) [3, 4]. His-
topathological analysis confirmed the protective effect
of TEO and GEO on ethanol-induced ulcer in rats. Alco-
hol-induced stress leads to changes in the stomach as
indicated by profuse submucosal hemorrhages, erosions
and petechiae, which were confirmed histopathologi-
cally as defects in mucosa and submucosal hemorrhages.
Essential oil administration restored all the histological
changes. These results indicate that TEO and GEO admin-
istration significantly enhance antioxidant enzymes such
as catalase, GPx, SOD and GSH present in gastric mucosa
and reduce gastric damage.
Acknowledgments: The authors thank Spices
Board, Cochin, India for providing funds (grant no.
MD/M&H/01/2008-09) to carry out this work.
Conflict of interest statement
Authors’ conflict of interest disclosure: The authors
stated that there are no conflicts of interest regarding the
publication of this article. Research funding played no
role in the study design; in the collection, analysis, and
interpretation of data; in the writing of the report; or in the
decision to submit the report for publication.
Research funding: The financial support for this work was
provided by Spices Board, Cochin, India.
Employment or leadership: None declared.
Honorarium: None declared.
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