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Table of Contents
ORIGINAL ARTICLE
Year : 2013  |  Volume : 1  |  Issue : 2  |  Page : 95-103

Protective effect of ethanolic extract of seeds of Coriandrum sativum l. in acetic acid-induced ulcerative colitis in male wistar rats


1 PG Student, Department of Pharmacology, Priyadarshini College of Pharmaceutical Sciences, Narapally, Chowdaryguda (V), Ghatkesar (M), R.R.District, 500088, Andhra Pradesh, India
2 Professor & Head, Department of Pharmacology, Priyadarshini College of Pharmaceutical Sciences, Narapally, Chowdaryguda (V), Ghatkesar (M), R.R.District, 500088, Andhra Pradesh, India

Date of Web Publication21-Aug-2018

Correspondence Address:
M Mohan
Professor & Head, Department of Pharmacology, Priyadarshini College of Pharmaceutical Sciences, Narapally, Chowdaryguda (V), Ghatkesar (M), R.R.District, 500088, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2347-6486.239502

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  Abstract 


Objective: To evaluate the protective effect of ethanolic extract of dried seeds of Coriandrum sativum L. (C.sativum) in acetic acid-induced ulcerative colitis in rats.
Methods: Male Wistar rats were divided into various treatment groups (n=5). The animals were administered with 2ml of acetic acid (4% v/v) via intrarectal route to induce colitis. Prednisolone (2mg/kg) was used as a standard drug and C.sativum was administered at a dose of 100 and 300 mg/kg p.o. Macroscopic scoring, colon weight to length ratio, colonic superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), lipid peroxidation (LPO), myeloperoxidase (MPO) levels and histopathological changes were recorded after the treatment regimen of 11 days.
Results: Intrarectal instillation of acetic acid caused significant (P<0.05) increase in colon weight to length ratio, LPO, and MPO levels; and significant (P<0.05) decrease in the levels of SOD, CAT and GSH levels. Pretreatment with C.sativum (100, 300 mg/kg, p.o.) exhibited significant (P<0.05) reversal of all the above biochemical parameters and significantly reversed the histopathological changes induced by acetic acid treatment.
Conclusion: The present investigation demonstrates the potent therapeutic value of C.sativum (100, 300 mg/kg, p.o.) in the amelioration of experimental colitis in rats. The beneficial effect of C.sativum could be attributed to its antioxidant effect.

Keywords: C.sativum, Acetic acid, Ulcerative colitis, antioxidant


How to cite this article:
Poojari S, Bhargavi R, Mohan M. Protective effect of ethanolic extract of seeds of Coriandrum sativum l. in acetic acid-induced ulcerative colitis in male wistar rats. J Integr Health Sci 2013;1:95-103

How to cite this URL:
Poojari S, Bhargavi R, Mohan M. Protective effect of ethanolic extract of seeds of Coriandrum sativum l. in acetic acid-induced ulcerative colitis in male wistar rats. J Integr Health Sci [serial online] 2013 [cited 2021 Nov 30];1:95-103. Available from: https://www.jihs.in/text.asp?2013/1/2/95/239502




  Introduction Top


Ulcerative colitis (UC) is an idiopathic Inflammatory Bowel Disease (IBD) characterized by cycles of acute inflammation, ulceration and bleeding of the colonic mucosa. IBD is a chronic, remitting relapsing disorder of the gastrointestinal tract characterized by inflammation and tissue damage. The etiology of the disease although not well understood, is thought to be multifactorial. Oxidative stress is one of the key biochemical features of the disease[1][2][3]. Various inflammatory mediators such as cyclooxygenases (COX-1 and COX-2), tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), and interleukin-12 (IL-12), the presence of highly activated inflammatory cells such as neutrophils, dendritic cells, macrophages, and excessive production of reactive oxygen species (ROS) have been implicated in the pathogenesis of the disease[4]. The use of medicinal plants or their active components is becoming an increasingly attractive approach for the treatment of various inflammatory disorders among patients unresponsive to or unwilling to take standard medicines. Among these alternative approaches is the use of food derivatives, which have the advantage of being relatively nontoxic. However, limited scientific evidence regarding the effectiveness of these natural derivatives, in conjunction with a lack of mechanistic understanding of their actions has prevented their incorporation into the mainstream of medical care.

During the last decade, a large number of dietary components have been evaluated as potential chemopreventive agents[5]. IBD patients turn to alternative therapies for various reasons, including side effects or lack of effectiveness of conventional therapies, fear of surgery, presumed safety and effectiveness of alternative treatments, or the simple desire to regain control of their deteriorating health.[6],[7]

Some medicinal plants reported to be effective in the treatment of UC include Azadirachta indica [8] Moringa olifera Lam.‘[9] Ginko biloba”[10], Hibiscus rosa sinensisLinn[11] and Curcuma longa[12]. Some traditional Chinese medicines aloe vera gel, wheat grass juice, Boswellia serrata, and bovine colostrums enemas in patients with ulcerative colitis have also been used[13].

Coriandrum sativum L. of family Umbelliferae, a glabrous aromatic, herbaceous annual plant is well known for its use as an antioxidant. Essential oil, flavonoids, fatty acids, and sterols have been isolated from different parts of C.sativum [14]. It is a soft, hairless plant growing up to 50cm in height and is native to Southwestern Asia and North Africa. All parts of the plant are edible but the fresh leaves and the dried seeds are the most eaten parts of the plant[15]. Coriander seed is a popular spice and finely ground seed is a major ingredient of curry powder. The seeds are mainly responsible for the medicinal use of coriander and have been used as a drug for indigestion, against worms, rheumatism and pain in the joints[16]. C.sativum is reported to have a very effective anti-oxidant activity profile showing 2, 2- diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity, lipooxygenase inhibition, and phospholidpid peroxidation inhibition, iron chelating activity, hydroxyl radical scavenging activity, superoxide dismutation, glutathione reduction and antilipid peroxidation[17]activities.

Phytochemical studies revealed the presence of constituents such as flavanoids (quercetin 3-glucoronide)[18], linalool, camphor, geranylacetate, geraniol[19], isocoumarins, coumarins and coriandrones[20]. Caffeic acid, protocatechinic acid, and glycitin were characterized as major polyphenolics of coriander[21]. It has also been reported to exhibit several other pharmacological effects such as antioxidant activity[22][23], anti-diabetic[24], anti- mutagenic [25], anthelmenthic [26], sedative-hypnotic[27], anticonvulsant [28], diuretic [29], cholesterol lowering[30], protective role against lead toxicity (31), anti^ngal activity[32], anti-feeding[33], anticancer [34], anxiolytic[35], hepatoprotective [36], anti-protozoal[37], anti-ulcer [38], post-coital anti-fertility[39] and heavy metal detoxification activities[40].

Several models of experimental colitis resembling UC have been reported previously. The most widely used models are induced by administering toxic chemicals such as dextran sulphate sodium (DSS)[41], trinitrobenzene sulfonic acid (TNBS)[42] and acetic acid[43]. In this a reproducible model of UC in male Wistar rats was developed by intrarectal administration of 2ml acetic acid (4% v/v). The role of C.sativum in the possible modulation of colon inflammation has not been verified. This prompted us to study the potential effects of ethanolic extract of seeds of C.sativum extract on experimental acetic acid-induced colitis in rats.


  Methods Top


2.1. Animals

Healthy adult male Wistar rats (180-200 g) were obtained from Mahavir Enterprises, Hyderabad, India. They were maintained at (24±1 °C), with relative humidity of 45-55% and 12:12 dark/light cycle. The animals were acclimatized for a period of one week. Commercial pellet diet and water were provided ad libitum. The experiments were carried out according to the guidelines of the committee for the purpose of control and supervision of experiments on animals (CPCSEA), New Delhi, India and approved by the Institutional Animal Ethical Committee (IAEC).

2.2. Plant material collection and preparation of extract

Dry seeds of C.sativum were purchased locally and authenticated from Department of Pharmacognosy, Priyadarshini College of Pharmaceutical Sciences, Hyderabad. Seeds were dried and made into fine powder. The powdered material (100g) was first defatted with petroleum ether (60-80 °C) using Soxhlet apparatus. The marc was dried and again extracted using ethanol for 24h. The extract was then collected and air dried to obtain the product (4.5% w/w). Appropriate concentrations of the extract were made using distilled water and polyethylene glycol (PEG) (1:1) as vehicle.

2.3.Preliminaryphytochemicalscreening

The preliminary phytochemical screening of ethanolic extract was tested for the presence of flavonoids, alkaloids, glycosides, tannins and saponins[44].

2.4. Standard drug

Prednisolone was obtained as a gift sample from Bafna Pharmaceuticals Ltd. (Chennai) and all other chemicals used were purchased locally.

2.5. Induction of colitis

Rats were fasted for 24 h. 2ml of 4% acetic acid was administered into the rectum of rats using 3mm diameter catheter at a distance of 8cms into colon for 30s. After 30s acetic acid was withdrawn followed by flushing of colon using 0.9% saline[45].

2.6. Treatment protocol

The animals were randomly divided into following experimental groups with 5 animals in each group.

Group 1 - Vehicle treated animals: received 1ml of distilled water and PEG (1:1) for 11days.

Group 2 - Acetic acid control animals: received 2ml of 4% (v/v) acetic acid solution, once intrarectally

Group 3 - Prednisolone treated animals: received Prednisolone (2mg/kg, p.o.) for 3days and acetic acid (2ml of 4% v/v solution, once intrarectally).

Prednisolone and acetic acid treatment was started on the same day.

Group 4 – Drug treated animals: Pre-treated with C.sativum (100mg/kg, p.o.) for 7days and 2ml of 4% acetic acid solution intra rectally on 8th day. Drug treatment was continued till 11th day.

Group 5 - Drug treated animals: Pre-treated with C.sativum (300mg/kg. p.o.) for 7days and 2ml of 4%acetic acid solution intrarectally on 8th day. Drug treatment was continued till 11thday.

On the 11th day animals were sacrificed and colons were collected for morphological and biochemical assays. Portions of colonic specimens were kept in 10% formalin solution for histopathological studies.

2.7. Assessment of colonic damage

2.7.1. Macroscopic scoring: The colon was excised and opened longitudinally, rinsed with ice-cold normal saline and colonic damage was evaluated according to scale ranging from 0 to 4 as follows[46]:

0 - Normal appearance; 1 - Mucosal erythema only; 2 - Mild edema, slight bleeding or small erosions

3 - Moderate edema, bleeding, ulcers; 4 - Severe ulcerations, erosions, edema and tissue necrosis

2.7.2. Colon weight/length ratio (g/cm): After animals were sacrificed colon was removed, gently flushed with ice-cold normal saline placed on ice cold plate, cleaned of fat and mesentery and blotted on filter paper to dry lightly. Each colon was weighed and its length was measured [47]. It was used as a parameter to assess the degree of colon edema which reflected the severity of colitis.

2.7.3. Estimation of colonic mucosal antioxidants (SOD, CAT, GSH, LPO) and pro-inflammatory marker –MPO)

2.7.3.1. Preparation of tissue homogenate

The colon tissue was washed with ice-cold saline and homogenized with 0.1M tris buffer (pH 7.5) using Remi homogenizer to give 10% homogenate. The homogenate was centrifuged at 10,000 rpm for 20 min and supernatant was used for estimation of antioxidant enzyme levels.

2.7.3.2. Superoxide dismutase activity (SOD)

The assay of SOD was based on ability of SOD to inhibit spontaneous oxidation of adrenaline to adrenochrome. 0.05ml supernatant was added to 2.0ml of carbonate buffer and 0.5ml of 0.01 Mm EDTA solutions. The reaction was initiated by addition of 0.5ml of epinephrine and autoxidation of adrenaline to adrenochrome was measured at 480nm. The change in absorbance for every minute was measured against blank. The results are expressed as unit of SOD activity (mg/wet tissue)[48].

2.7.3.3.Catalase activity (CAT)

The reaction mixture consisted of 2ml of phosphate buffer (pH 7.0), 0.95ml of hydrogen peroxide (0.019M) and 0.05ml of supernatant in a final volume of 3ml.Absorbance was recorded at 240nm every 10sec for 1min. One unit of CAT was defined as the amount of enzyme required to decompose 1μmol of peroxide per min at 25 ° C .The results were expressed as units of CAT U/g of wet tissue [49].

2.7.3.4. Reduced Glutathione (GSH)

1ml of homogenate is added to 1ml of 10% TCA and centrifuged.1ml of supernatant is treated with 0.5ml of Ellman’s reagent (19.8 mg of 5,5’-dithiobisnitro benzoic acid (DTNB) in 100ml of 1% sodium citrate) and 3ml of phosphate buffer (pH-8). The color developed was measured at 412nm [5]”.

2.7.3.5. Lipid peroxidation (LPO)

In brief, 0.1ml of homogenate (Tris-HCl buffer, ph 7.5) was treated with 2ml of (1:1:1) TBA-TCA-HCl reagent (Thiobarbituric acid 0.37%, 0.25N HCl and 15% TCA) and placed in water bath for 15 min, cooled and centrifuged at room temperature for 10 min at 1000 rpm. The absorbance of clear supernatant was measured against reference blank at 535nm[51].

2.7.3.6. Myeloperoxidase (MPO)

0.1ml of homogenate (Tris Hcl buffer, pH 7.5) was treated with equal volume of potassium phosphate buffer (pH 7.5) and was centrifuged at room temperature for 10 min at 10000 rpm. The supernatant was treated with 0.5% tetramethylbenzidine. This mixture was oxidized by MPO in presence of hydrogen peroxide and absorbance was measured at

655 nm[52].

2.7.4. Histopathological examination

The colonic tissues were fixed in 10% formalin. The specimens were then processed for standard procedure and were embedded in paraffin wax in Swiss roll model to expose the lesional and normal areas of colon tissue. The blocks were then sectioned according to hematoxylin and eosin method [53]. Five-micrometer thick histological sections were obtained from the paraffin blocks. The sections were examined under the light microscope and photographs were taken under 40X.

2.8. Statistical analysis

All data were expressed as the mean ± SEM. For statistical analysis of the data, group means were compared by one-way analysis of variance (ANOVA) followed by Dunnett’s test P<0.05 was considered significant.


  Results Top


3.1. Preliminary phytochemical screening

The ethanolic extract of Coriandrum sativum L. was found to contain flavonoids, alkaloids, glycosides, tannins and saponins.

3.2. Macroscopic results

The acetic acid treatment induced severe macroscopic inflammation in the colon after rectal administration as assessed by the colonic damage score [Table 1]. Treatment with Prednisolone significantly reduced the severity of the tissue damage. C.sativum (100, 300mg/kg) significantly reduced the intensity of inflammation in a dose-dependent manner as shown [Table 1]. Acetic acidinduced colitis produced diarrhoea in all the animals whereas none of the animals in the vehicle treated group had diarrhoea. Administration of C.sativum (100, 300mg/kg) reduced the frequency of diarrhoea in experimental colitis (data not shown).
Table 1: Effect of C.sativum (100 and 300mg/kg) on colon weight to length ratio (g/cm) and macroscopic scoring of rats in acetic acid-induced ulcerative colitis (n=5) (Mean±SEM).

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3.3. Effect of colonic SOD activity

There was a significant (P<0.05) decrease in colonic SOD activity in rats given acetic acid treatment only as compared to vehicle treated group. Pretreatment of rats with C.sativum (at doses of 100 and 300 mg/kg) orally caused a significant (P<0.05) increase in colitis-induced reduction of SOD activity, [Table 2].
Table 2: Effect of C.sativum (100 and 300mg/kg) on colon weight to length ratio (g/cm) and macroscopic scoring of rats in acetic acid-induced ulcerative colitis (n=5) (Mean±SEM)

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All data analyzed by one way ANOVA followed by Dunnet’s test. *P<0.05 as compared to vehicle treated group, #P<0.05 as compared to acetic acid control group.

(0-normal appearance; 1- mucosal erythema only; 2- mild oedema, slight bleeding or small erosions; 3- moderate oedema, bleeding, ulcers; 4-severe ulcerations, erosions, oedema and tissue necrosis)

3.4. Effect of colonic Catalase activity

Tissue catalase levels decreased significantly (P<0.05) following intrarectal administration of acetic acid compared to vehicle treated group. Pretreatment of rats with C.sativum (300 mg/kg) orally caused a significant (P<0.05) increase in catalase activity as compared with acetic acid control group. On the other hand the effect of C.sativum (100mg/kg) was similar to Prednisolone control (2mg/kg) [Table 2].{Table 2}

3.5. Effect of colonic GSH levels

[Table 2] illustrates that tissue GSH levels was significantly (P<0.05) decreased after induction of colitis as compared to vehicle treated group. Treatment with Prednisolone (2mg/kg) or C.sativum (100 & 300mg/kg) showed a significant increase in the GSH levels. The increase was significantly (P<0.05) higher with C.sativum at a dose of 300mg/kg.

3.6. Effect of colonic lipid peroxidation

Tissue LPO activity showed a statistically significant (P<0.05) increase in acetic acid treated group as compared to the vehicle treated group. Treatment with Prednisolone (2mg/kg, p.o.) and C.sativum (100 and 300mg/kg) significantly reduced colonic LPO activity [Table 2].

3.7. Effect on colonic myeloperoxidase

Tissue MPO activity showed a significant (P<0.05) increase in acetic acid treated group as compared to the vehicle treated group. Treatment with C.sativum (100 and 300mg/kg) significantly reduced colonic MPO activity [Table 2].

All data analyzed by one way ANOVA followed by Dunnet’s test. *P<0.05 as compared to vehicle treated group, #P<0.05 as compared to acetic acid group.

3.8. Histopathological examination

Histopathological examination (40X) of colon tissue of rats treated with acetic acid (4%) showed significant cell inflammation with loss of mucosa (30%), whereas C. sativum (100mg/kg) showed scattered round cell collection in mucosa and submucosa, and C. sativum (300mg/kg) showed near to normal architecture [Figure 1].
Figure 1: Photomicrographs of histopathological examination (40X) of colon tissue. Section A) Control group treated with vehicle shows normal architecture, section B) group treated with acetic acid (4% v/v) shows significant cell inflammation, loss of mucosa (30%), section C) group treated with Prednisolone (2mg/kg) shows scattered round cell collection in mucosa and submucosa, section D) group treated with C.sativum extract (100mg/kg) shows loss of mucosa (10%), section E) group treated with C.sativum extract (300mg/kg) shows near to normal architecture.


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  Discussion And Conclusion Top


The use of plants with herbal healing properties is as old as mankind as they have been used since antiquity in treating various diseases of man. The present study evaluated the protective effect of ethanolic extract of seeds of Coriandrum sativum in acetic acid-induced UC in male Wistar rats.

Acetic acid induced colitis model is similar to human ulcerative colitis in terms of histopathological features. It affects the distal colon portion and induces non-transmural inflammation, massive necrosis of mucosal and sub-mucosal layers, mucosal edema, neutrophil infiltration of the mucosa and submucosal ulceration. The protonated form of the acid liberates protons within the intracellular space and causes massive intracellular acidification resulting in massive epithelial damage. Inflammation is the pathogenesis of IBD, and several pathways are associated with inflammatory response in IBD due to mucosal intestinal flora[54]. The inflammatory response initiated by acetic acid includes activation of cyclooxygenase and lipooxygenase pathways[55],[56].

The most disabling feature of UC, is the episodic acute exacerbation. During these periods, there is an association between acute inflammation (presence of neutrophils), tissue damage and diarrhoea. Administration of acetic acid significantly increased colon weight and incidence of diarrhoea which is in agreement with earlier reports [57],[58]. Pre-treatment with ethanolic extract of seeds of C.sativum (100 and 300mg/kg) exhibited a decrease in the colon weight and incidence of diarrhoea.

The gross morphological lesions characterized by ulcer and necrotic area of various sizes, were healed depicting protection from the corrosive effect of acetic acid by ethanolic extract of seeds of C.sativum. Oxidative stress also has been implicated in the pathogenesis of UC in experimental animals [59]. Excess production of reactive oxygen metabolites e.g., superoxide, hydroxyl radical, hydrogen peroxide, hypochlorous acid and oxidant derivatives are detected in inflamed mucosa and may be pathogenic in IBD [6]. Intestinal mucosal damage in the IBD is related to both increased free radical production and a low concentration of endogenous antioxidant defense [61].

We estimated SOD, Catalase, GSH, and LPO levels in addition to morphological changes in the colonic tissue as an index to assess the severity of oxidative damage. Pretreatment with C.sativum (100mg/kg and 300mg/kg, p.o.) exhibited significant (P<0.05) reversal of all the above biochemical parameters and reversed the histopathological changes induced by acetic acid treatment. The colonic

MPO activity, an index of neutrophil activation and inflammation was increased in acetic acid-treated animals. Activated neutrophils pass out of the circulation and enter the inflamed mucosa and submucosa of the large intestine during acute inflammation, leading to overproduction of reactive oxygen and nitrogen species that contribute to intestinal injury [62]. This increase in MPO activity was significantly reduced in rats treated with C.sativum extract (100mg/kg and 300mg/kg.)

The histopathological examination of colon tissue showed significant cell inflammation and 30% loss of mucosa in acetic acid-treated group whereas tissue treated with C.sativum extract(100mg/kg) showed 10% loss of mucosa; and that treated with C.sativum extract(300mg/kg) showed near normal architecture.

The results showed that ethanolic extract of seeds of Coriandrum sativum has significant protective activity against experimental colitis in rats, as indicated by its morphological, biochemical and histopathological studies. Thus in conclusion, ethanolic extract of C.sativum (100 and 300mg/kg) has ameliorated the effects of acetic acid in Wistar rats by way of normalizing the damaged tissue, resetting the antioxidant levels and reversing the histopathological changes induced by dose dependent acetic acid.


  Acknowledgment Top


The authors acknowledge the technical assistance provided by Dr.P.Uday kumar, Scientist E (Deputy Director) & HOD, Pathology Division, NIN (ICMR), Tarnaka, Hyderabad, Andhra Pradesh, India for histopathology study and its critical evaluation.



 
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