Inside pages - 19-04-14

The Journal of
Integrated Health Sciences
Available online at Protective effect of ethanolic extract of seeds of Coriandrum sativum l. in acetic acid-induced
ulcerative colitis in male wistar rats

S.Poojari , R.Bhargavi , M. Mohan1,2 PG Student; Professor & Head, Department of Pharmacology, Priyadarshini College of Pharmaceutical Sciences, Narapally, Chowdaryguda (V), Ghatkesar (M), R.R.District, 500088, Andhra Pradesh 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.
Key Words: C.sativum, Acetic acid, Ulcerative colitis, antioxidant
patients unresponsive to or unwilling to take standard medicines. Among these alternative approaches is the Ulcerative colitis (UC) is an idiopathic Inflammatory use of food derivatives, which have the advantage of Bowel Disease (IBD) characterized by cycles of acute being relatively nontoxic. However, limited scientific inflammation, ulceration and bleeding of the colonic evidence regarding the effectiveness of these natural mucosa. IBD is a chronic, remitting relapsing derivatives, in conjunction with a lack of mechanistic disorder of the gastrointestinal tract characterized by understanding of their actions has prevented their inflammation and tissue damage. The etiology of the incorporation into the mainstream of medical care. disease although not well understood, is thought to be During the last decade, a large number of dietary multifactorial. Oxidative stress is one of the key components have been evaluated as potential biochemical features of the disease . Various chemopreventive agents . IBD patients turn to inflammatory mediators such as cyclooxygenases alternative therapies for various reasons, including (COX-1 and COX-2), tumor necrosis factor-alpha side effects or lack of effectiveness of conventional (TNF-a), interleukin-6 (IL-6), and interleukin-12 therapies, fear of surgery, presumed safety and (IL-12), the presence of highly activated effectiveness of alternative treatments, or the simple inflammatory cells such as neutrophils, dendritic desire to regain control of their deteriorating health.
cells, macrophages, and excessive production of reactive oxygen species (ROS) have been implicated Some medicinal plants reported to be effective in the in the pathogenesis of the disease . The use of treatment of UC include Azadirachta indica , medicinal plants or their active components is Moringa olifera Lam. , Ginko biloba , Hibiscus rosa becoming an increasingly attractive approach for the sinensis Linn and Curcuma longa . Some traditional treatment of various inflammatory disorders among Chinese medicines aloe vera gel, wheat grass juice, Boswellia serrata, and bovine colostrums enemas in patients with ulcerative colitis have also been used .
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 Coriandrum sativum L. of family Umbelliferae, a obtained from Mahavir Enterprises, Hyderabad, glabrous aromatic, herbaceous annual plant is well India. They were maintained at (24±1 °C), with known for its use as an antioxidant. Essential oil, relative humidity of 45-55% and 12:12 dark/light flavonoids, fatty acids, and sterols have been isolated cycle. The animals were acclimatized for a period of from different parts of C.sativum . It is a soft, one week. Commercial pellet diet and water were hairless plant growing up to 50cm in height and is provided ad libitum. The experiments were carried native to Southwestern Asia and North Africa. All out according to the guidelines of the committee for parts of the plant are edible but the fresh leaves and the purpose of control and supervision of experiments the dried seeds are the most eaten parts of the plant . on animals (CPCSEA), New Delhi, India and Coriander seed is a popular spice and finely ground approved by the Institutional Animal Ethical seed is a major ingredient of curry powder. The seeds Committee (IAEC).
are mainly responsible for the medicinal use of 2.2. Plant material collection and preparation of coriander and have been used as a drug for indigestion, against worms, rheumatism and pain in the joints . C.sativum is reported to have a very Dry seeds of C.sativum were purchased locally and effective anti-oxidant activity profile showing 2, 2- authenticated from Department of Pharmacognosy, diphenyl-1-picrylhydrazyl (DPPH) radical Priyadarshini College of Pharmaceutical Sciences, scavenging activity, lipooxygenase inhibition, and Hyderabad. Seeds were dried and made into fine phospholidpid peroxidation inhibition, iron chelating powder. The powdered material (100g) was first activity, hydroxyl radical scavenging activity, defatted with petroleum ether (60-80 ºC) using superoxide dismutation, glutathione reduction and Soxhlet apparatus. The marc was dried and again antilipid peroxidation activities. extracted using ethanol for 24h. The extract was then collected and air dried to obtain the product (4.5% Phytochemical studies revealed the presence of w/w). Appropriate concentrations of the extract were constituents such as flavanoids (quercetin 3- made using distilled water and polyethylene glycol glucoronide) , linalool, camphor, geranylacetate, (PEG) (1:1) as vehicle.
coriandrones . Caffeic acid, protocatechinic acid, 2.3. Preliminary phytochemical screening and glycitin were characterized as major The preliminary phytochemical screening of polyphenolics of coriander . It has also been reported ethanolic extract was tested for the presence of to exhibit several other pharmacological effects such flavonoids, alkaloids, glycosides, tannins and as antioxidant activity , anti-diabetic , anti- mutagenic , anthelmenthic , sedative-hypnotic , 2.4. Standard drug anticonvulsant , diuretic , cholesterol lowering , protective role against lead toxicity Prednisolone was obtained as a gift sample from activity , anti-feeding , anticancer , anxiolytic , Bafna Pharmaceuticals Ltd. (Chennai) and all other hepatoprotective , anti-protozoal , anti-ulcer , chemicals used were purchased locally.
post-coital anti-fertility and heavy metal 2.5. Induction of colitis detoxification activities .
Rats were fasted for 24 h. 2ml of 4% acetic acid was Several models of experimental colitis resembling administered into the rectum of rats using 3mm UC have been reported previously. The most widely diameter catheter at a distance of 8cms into colon for used models are induced by administering toxic 30s. After 30s acetic acid was withdrawn followed by chemicals such as dextran sulphate sodium (DSS) , flushing of colon using 0.9% saline .
trinitrobenzene sulfonic acid (TNBS) and acetic acid . In this a reproducible model of UC in male 2.6. Treatment protocol Wistar rats was developed by intrarectal The animals were randomly divided into following administration of 2ml acetic acid (4% v/v). The role experimental groups with 5 animals in each group.
of C.sativum in the possible modulation of colon inflammation has not been verified. This prompted us Group 1 - Vehicle treated animals: received 1ml to study the potential effects of ethanolic extract of of distilled water and PEG (1:1) for 11days.
seeds of C.sativum extract on experimental acetic Group 2 - Acetic acid control animals: received acid-induced colitis in rats. 2ml of 4% (v/v) acetic acid solution, once Group 3 - Prednisolone treated animals: received 2.1. Animals Prednisolone (2mg/kg, p.o.) for 3days and acetic Healthy adult male Wistar rats (180-200 g) were acid (2ml of 4% v/v solution, once intrarectally). The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 Prednisolone and acetic acid treatment was unit of SOD activity (mg/wet tissue) . started on the same day. Catalase activity (CAT) Group 4 – Drug treated animals: Pre-treated with The reaction mixture consisted of 2ml of phosphate C.sativum (100mg/kg, p.o.) for 7days and 2ml of buffer (pH 7.0), 0.95ml of hydrogen peroxide 4% acetic acid solution intra rectally on 8 day. (0.019M) and 0.05ml of supernatant in a final Drug treatment was continued till 11 day.
volume of 3ml.Absorbance was recorded at 240nm Group 5 - Drug treated animals: Pre-treated with every 10sec for 1min. One unit of CAT was defined as C.sativum (300mg/kg. p.o.) for 7days and 2ml of the amount of enzyme required to decompose 1µmol 4%acetic acid solution intrarectally on 8th day. of peroxide per min at 25 ° C .The results were Drug treatment was continued till 11 day.
expressed as units of CAT U/g of wet tissue .
On the 11 day animals were sacrificed and colons Reduced Glutathione (GSH) were collected for morphological and biochemical 1ml of homogenate is added to 1ml of 10% TCA and assays. Portions of colonic specimens were kept in centrifuged.1ml of supernatant is treated with 0.5ml 10% formalin solution for histopathological studies.
of Ellman's reagent (19.8 mg of 5,5'-dithiobisnitro 2.7. Assessment of colonic damage benzoic acid (DTNB) in 100ml of 1% sodium citrate) and 3ml of phosphate buffer (pH-8). The color 2.7.1. Macroscopic scoring: The colon was excised developed was measured at 412nm .
and opened longitudinally, rinsed with ice-cold normal saline and colonic damage was evaluated Lipid peroxidation (LPO) according to scale ranging from 0 to 4 as follows : In brief, 0.1ml of homogenate (Tris-HCl buffer, ph 0 - Normal appearance; 1 - Mucosal erythema only; 2 7.5) was treated with 2ml of (1:1:1) TBA-TCA-HCl - Mild edema, slight bleeding or small erosions reagent (Thiobarbituric acid 0.37%, 0.25N HCl and 15% TCA) and placed in water bath for 15 min, 3 - Moderate edema, bleeding, ulcers; 4 - Severe cooled and centrifuged at room temperature for 10 ulcerations, erosions, edema and tissue necrosis min at 1000 rpm. The absorbance of clear supernatant 2.7.2. Colon weight/length ratio (g/cm): After was measured against reference blank at 535nm .
animals were sacrificed colon was removed, gently Myeloperoxidase (MPO) flushed with ice-cold normal saline placed on ice cold plate, cleaned of fat and mesentery and blotted on 0.1ml of homogenate (Tris Hcl buffer, pH 7.5) was filter paper to dry lightly. Each colon was weighed treated with equal volume of potassium phosphate and its length was measured . It was used as a buffer (pH 7.5) and was centrifuged at room parameter to assess the degree of colon edema which temperature for 10 min at 10000 rpm. The supernatant reflected the severity of colitis.
was treated with 0.5% tetramethylbenzidine. This mixture was oxidized by MPO in presence of 2.7.3. Estimation of colonic mucosal antioxidants hydrogen peroxide and absorbance was measured at (SOD, CAT, GSH, LPO) and pro-inflammatory marker –MPO) 2.7.4. Histopathological examination Preparation of tissue homogenate The colonic tissues were fixed in 10% formalin. The The colon tissue was washed with ice-cold saline and specimens were then processed for standard homogenized with 0.1M tris buffer (pH 7.5) using procedure and were embedded in paraffin wax in Remi homogenizer to give 10% homogenate. The Swiss roll model to expose the lesional and normal homogenate was centrifuged at 10,000 rpm for 20 areas of colon tissue. The blocks were then sectioned min and supernatant was used for estimation of according to hematoxylin and eosin method . Five- antioxidant enzyme levels.
micrometer thick histological sections were obtained Superoxide dismutase activity (SOD) from the paraffin blocks. The sections were examined under the light microscope and photographs were The assay of SOD was based on ability of SOD to taken under 40X. inhibit spontaneous oxidation of adrenaline to adrenochrome. 0.05ml supernatant was added to 2.8. Statistical analysis 2.0ml of carbonate buffer and 0.5ml of 0.01 Mm All data were expressed as the mean ± SEM. For EDTA solutions. The reaction was initiated by statistical analysis of the data, group means were addition of 0.5ml of epinephrine and autoxidation of compared by one-way analysis of variance (ANOVA) adrenaline to adrenochrome was measured at 480nm. followed by Dunnett's test P<0.05 was considered The change in absorbance for every minute was measured against blank. The results are expressed as The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 dependent manner as shown (Table I). Acetic acid-induced colitis produced diarrhoea in all the animals 3.1. Preliminary phytochemical screening whereas none of the animals in the vehicle treated The ethanolic extract of Coriandrum sativum L. was group had diarrhoea. Administration of C.sativum found to contain flavonoids, alkaloids, glycosides, (100, 300mg/kg) reduced the frequency of diarrhoea tannins and saponins.
in experimental colitis (data not shown).
3.2. Macroscopic results 3.3. Effect of colonic SOD activity The acetic acid treatment induced severe There was a significant (P<0.05) decrease in colonic macroscopic inflammation in the colon after rectal SOD activity in rats given acetic acid treatment only administration as assessed by the colonic damage as compared to vehicle treated group. Pretreatment of score (Table I). Treatment with Prednisolone significantly reduced the severity of the tissue rats with C.sativum (at doses of 100 and 300 mg/kg) damage. C.sativum (100, 300mg/kg) significantly orally caused a significant (P<0.05) increase in reduced the intensity of inflammation in a dose- colitis-induced reduction of SOD activity, (Table II). 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).
Macroscopic Colon weight :
Vehicle (1ml/kg) 0.0±0.00 control (2ml of 4% v/v)Prednisolone (2mg/kg)C.sativum (100mg/kg)C.sativum All data analyzed by one way ANOVA followed by significantly (P<0.05) decreased after induction of Dunnet's test. P<0.05 as compared to vehicle treated colitis as compared to vehicle treated group. group, P<0.05 as compared to acetic acid control Treatment with Prednisolone (2mg/kg) or C.sativum (100 & 300mg/kg) showed a significant increase in the GSH levels. The increase was significantly (0-normal appearance; 1- mucosal erythema only; 2- mild oedema, slight bleeding or small erosions; 3- (P<0.05) higher with C.sativum at a dose of moderate oedema, bleeding, ulcers; 4-severe ulcerations, erosions, oedema and tissue necrosis) 3.6. Effect of colonic lipid peroxidation 3.4. Effect of colonic Catalase activity Tissue LPO activity showed a statistically significant Tissue catalase levels decreased significantly (P<0.05) increase in acetic acid treated group as (P<0.05) following intrarectal administration of compared to the vehicle treated group. Treatment acetic acid compared to vehicle treated group. with Prednisolone (2mg/kg, p.o.) and C.sativum (100 Pretreatment of rats with C.sativum (300 mg/kg) and 300mg/kg) significantly reduced colonic LPO orally caused a significant (P<0.05) increase in activity (Table II).
catalase activity as compared with acetic acid control 3.7. Effect on colonic myeloperoxidase group. On the other hand the effect of C.sativum (100mg/kg) was similar to Prednisolone control Tissue MPO activity showed a significant (P<0.05) (2mg/kg) (Table II).
increase in acetic acid treated group as compared to the vehicle treated group. Treatment with C.sativum 3.5. Effect of colonic GSH levels (100 and 300mg/kg) significantly reduced colonic Table II illustrates that tissue GSH levels was MPO activity (Table II).
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 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).

Reduced GSH
MPO (U/mg of
(U/mg of wet
(U/mg of wet
(ìg GSH/mg of (n moles/ mg of wet tissue)
wet tissue)
wet tissue)
(2mg/kg)C.sativum (100mg/kg)C.sativum 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 mucosal intestinal flora . The inflammatory response Histopathological examination (40X) of colon tissue initiated by acetic acid includes activation of of rats treated with acetic acid (4%) showed cyclooxygenase and lipooxygenase pathways significant cell inflammation with loss of mucosa The most disabling feature of UC, is the episodic (30%), whereas C. sativum (100mg/kg) showed acute exacerbation. During these periods, there is an scattered round cell collection in mucosa and association between acute inflammation (presence of submucosa, and C. sativum (300mg/kg) showed near neutrophils), tissue damage and diarrhoea. to normal architecture (Figure 1) Administration of acetic acid significantly increased DISCUSSION AND CONCLUSION
colon weight and incidence of diarrhoea which is in agreement with earlier reports . Pre-treatment with The use of plants with herbal healing properties is as ethanolic extract of seeds of C.sativum (100 and old as mankind as they have been used since antiquity 300mg/kg) exhibited a decrease in the colon weight in treating various diseases of man. The present study and incidence of diarrhoea.
evaluated the protective effect of ethanolic extract of seeds of Coriandrum sativum in acetic acid-induced The gross morphological lesions characterized by UC in male Wistar rats. ulcer and necrotic area of various sizes, were healed depicting protection from the corrosive effect of Acetic acid induced colitis model is similar to human acetic acid by ethanolic extract of seeds of C.sativum. ulcerative colitis in terms of histopathological Oxidative stress also has been implicated in the features. It affects the distal colon portion and pathogenesis of UC in experimental animals . induces non-transmural inflammation, massive Excess production of reactive oxygen metabolites necrosis of mucosal and sub-mucosal layers, mucosal e.g., superoxide, hydroxyl radical, hydrogen edema, neutrophil infiltration of the mucosa and sub- peroxide, hypochlorous acid and oxidant derivatives mucosal ulceration. The protonated form of the acid are detected in inflamed mucosa and may be liberates protons within the intracellular space and causes massive intracellular acidification resulting in pathogenic in IBD . Intestinal mucosal damage in massive epithelial damage. Inflammation is the the IBD is related to both increased free radical pathogenesis of IBD, and several pathways are production and a low concentration of endogenous associated with inflammatory response in IBD due to antioxidant defense . The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 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.
We estimated SOD, Catalase, GSH, and LPO levels in histopathological studies. Thus in conclusion, addition to morphological changes in the colonic ethanolic extract of C.sativum (100 and 300mg/kg) tissue as an index to assess the severity of oxidative has ameliorated the effects of acetic acid in Wistar rats damage. Pretreatment with C.sativum (100mg/kg and by way of normalizing the damaged tissue, resetting 300mg/kg, p.o.) exhibited significant (P<0.05) the antioxidant levels and reversing the reversal of all the above biochemical parameters and histopathological changes induced by dose reversed the histopathological changes induced by dependent acetic acid.
acetic acid treatment. The colonic MPO activity, an index of neutrophil activation and The authors acknowledge the technical assistance inflammation was increased in acetic acid-treated provided by Dr.P.Uday kumar, Scientist E (Deputy animals. Activated neutrophils pass out of the Director) & HOD, Pathology Division, NIN (ICMR), circulation and enter the inflamed mucosa and Tarnaka, Hyderabad, Andhra Pradesh, India for submucosa of the large intestine during acute histopathology study and its critical evaluation.
inflammation, leading to overproduction of reactive oxygen and nitrogen species that contribute to intestinal injury . This increase in MPO activity was significantly reduced in rats treated with C.sativum 1. Kokoszka J and Nelson RL. Determination of inflammatory bowel disease activity by breath extract (100mg/kg and 300mg/kg.) pentane analysis. Dis.Colon Rectum 1993; 36:
The histopathological examination of colon tissue showed significant cell inflammation and 30% loss of mucosa in acetic acid-treated group whereas tissue 2. Fiocchi C. Inflammatory bowel disease: etiology and pathogenesis. Gastroenterology 1998; 115:
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.
3. D'Odorico A, Bortolan S, Cardin R, D'Inca R, Martines D, Ferronato A & Sturniolo GC. The results showed that ethanolic extract of seeds of Reduced plasma antioxidant concentrations and Coriandrum sativum has significant protective activity against experimental colitis in rats, as inflammatory bowel disease. Scand J indicated by its morphological, biochemical and Gastroenterol 2001; 36: 1289-1294.
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 4. Xavier RJ and Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. phytopharmaceuticals. Stuttgart: Medpharm Nature 2007; 448(7152): 427-434.
GmbH Scientific Publishers; 1994.
5. Sharma S, Strutzman JD, Kellof GJ and Steele 17. Helle Wangensteen, Anne Berit Samuelsen, Karl VE. Screening of potential chemopreventive Egil Malterud. Antioxidant activity in agents using biochemical markers of extractsfrom coriander. Food Chem, 2004; 88(2):
carcinogenesis. Cancer Res 1994; 54: 5848-
18. Kunzemann J, Herrmann K. Isolation and 6. Hilsden RJ, Meddings JB, and Verhoef MJ. identification of flavon(ol)-O-glycosides in Complementary and alternative medicine use by caraway (carum carvi L.), Fennel (Foenticulum patients with inflammatory bowel disease: an vulgare Mill.), Anise (Pimpinella anisum L.) and Internet survey. Can J Gastroenterol 1999; 13:
coriander (Coriandrum sativum L.) and of flavon-C-glycosides in anise. I. phenolics of 7. Rawsthorne P, Shanahan F, Cronin NC, Anton species (author's transI) Z. Lebensm Unters PA, Lofberg R, Bohman L, and Bernstein CN. An Forsch 1977; 164: 194.
international survey of the use and attitudes 19. Karlsen J, Chingova B, Zwetkov R, Baerheim-S regarding alternative medicine by patients with vendsren A. Studies on the essential oil of the inflammatory bowel disease. Am J Gastroenterol fruits of Coriandrum sativum L. by means of gas 1999; 94: 1298-1303.
liquid chromatography ? ?. Studies on terpenes 8. Ghatule RR, Goel Shalini, Gautam MK, Singh A, and related compounds. Pharmaceut Weekbl Joshi VK and Goel RK. Effect of Azadirachta 1971; 106: 296.
indica leaves extract on acetic acid-induced 20 Taniguchi M Yanai M Xiao YQ Kido T Baba K colitis in rats: Role of antioxidants, free radicals Three isocoumarins from Coriandrum sativium and myeloperoxidase. Asian Pac J Trop Dis 2012; S651-S657.
L Photochemistry 1996 42 843
9. Swarnamoni Das and Lalit Kanodia. Effect of ethanolic extract of leaves of Moringa olifera Characterisation of antioxidant compounds in Lam. on acetic acid-induced colitis in albino rats. aqueous coriander extract Coriandrum sativum Asian J Pharm Clin Res 2012; 3(5): 110-114.
Food Sci Technol 2005 38 15 19
10. Ali Mustafa, Azza El-Medany, Hanan H Hagar, 22. Wangensteen H, Samuelsen AB, Malterud KE. Gamila El-Medany. Gingko biloba attenuates Antioxidant activity in extracts from coriander. mucosal damage in a rat model of ulcerative Food Chem 2004; 88:293-297.
colitis. Pharm Res 2006; 53: 324-330.
23. Deepa B, Anuradha CV. Antioxidant potential of 11. Amit D, Kiran S, Pinaki Ghosh. Effect of Coriandrum sativum L. seed extract. Ind J Expt hydroalcoholic extract of Hibiscus rosa sinensis Biol 2011; 49: 30-38.
leaves in experimental colitis in rats. Asian Pac J Trop Biomed 2012; 337-344.
24. Matasyoh JC, Maiyo ZC, Ngure RM, Chepkorir R. Chemical composition and antimicrobial 12. Mithun Vishwanath K, Amit D, Sucheta D. Effect activity of the essential oil of Coriandrum of aqueous extract of Curcumis sativus sativum. Food Chem 2009; 113: 526-529.
fruit in ulcerative colitis in laboratory animals. Asian Pac J Trop Biomed 2012; S962-S969.
25. Cortes-Eslava J, Gomez-Arroyo S, Villalobos- Pietrini R. Antimutagenicity of coriander 13. Langmead L, Rampton DS. Review article: (Coriandrum sativum) juice on the mutagenesis complementary and alternative therapies for produced by plant metabolites of aromatic inflammatory bowel disease. Aliment Pharmacol amines. Toxicol Lett 2004; 153: 283-292.
Ther 2006; 23: 341-349.
26. Eguale T, Tilahun G, Debella A, Feleke A, 14. Coriander- Coriandrum sativum L. by Axel Makonnen E. Invitro and invivo anthelmintic Diederchisen, Promoting the conservation and activity of crude extracts of Coriandrum sativum use of unutilized and neglected plants 2008; 8- against Haemonchus contortus. J Ethnopharmacol 2007; 110: 428-433.
15. Burdock GA, Carabin IG. Safety assessment of 27. Emamghoreishi M, Heidari-Hamedani G. coriander (Coriandrum sativum L.) essential oil Sedative-Hypnotic Activity of Extracts and as a food ingredient. Food Chem Toxicol. 2009; Essential Oil of Coriander Seeds. Iran J Med Sci 47: 22-34.
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 28. Hosseinzadeh H, Madanifard M. Anticonvulsant Coriandrum sativum in rats. J Ethnopharmacol effect of Coriandrum sativum L. seed Extracts in 1987; 21: 165-173.
mice. Iran J Pharm 2005; 3: 1-4.
40. Karunasagar D, Balaram Krishna MV, Rao SV, 29. Abderahim A, El-Hilaly J, Israili ZH, Lyoussi B. Arunachalam J. Removal and preconcentration Acute diuretic effect of continuous intravenous of inorganic and methyl mercury from aqueous infusion of an aqueous extract of Coriandrum media using a sorbent prepared from the plant Coriandrum sativum. J Hazard Mater 2005; 118:
Ethnopharmacol 2008; 115: 89-95.
30. Dhanapakiam P, Joseph JM, Ramaswamy VK. 41. Gaudio E, Taddei G, Vetuschi A, Sferra R, Frieri The cholesterol lowering property of coriander G, Ricciardi G. Dextran sulfate sodium (DSS) seeds (Coriandrum sativum). Mechanism of colitis in rats. Clinical, structural, and action. J Environ Biol 2008; 29(1): 53-56.
ultrastructural aspects. Dig. Dis. Sci.1999; 44(7):
31. Leena K, Veena S, Arti S. Protective role of Coriandrum sativum (coriander) extracts against 42. Morris GP, Beck PL, Herridge MS, Depew WT, lead nitrate induced oxidative stress and tissue Szewczuk MR, Wallace JL. Hapten-induced damage in the liver and kidney in male mice. Int J model of chronic inflammation and ulceration in Appl Biol Pharm Technol 2011; 2(3): 65-83.
the rat colon. Gastroenterology 1989; 96(3): 795-
32. Filomena S, Susana F, Andreia D. Antifungal activity of Coiandrum sativum essential oil, its 43. Millar AD, Rampton DS, Chander CL, Claxson mode of action against Candida species and AWD, Blake DR. Evaluating the antioxidant potential synergism with amphotericin B. potential of new treatments for inflammatory Phytomedicine 2011; 1-6.
bowel disease in a rat model of colitis. Gut 1996;
39: 407-415.
33. Catherine JD, Ian FH, Peter W, Lucy DL. Action of extracts of apiaceae on feeding behavior and 44. Kokate CK, Purohit AP, Gokhale SB. neurophysiology of the field slug Deroceras Pharmacognosy. In: Pathway to screen reticulatum. J ChemEcol 1999; 25(9): 2127-
phytochemical nature of natural drugs: 45th edition. Niral publication 2010; A1-A6.
34. Chithra V, Leelamma S. Coriandrum sativum – 45. Ghaneya SH, Soliman GA Design, synthesis and effect on lipid metabolism in 1, 2-dimethyl anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative Ethnopharmacol 2000; 71: 457-463.
colitis. European Journal of Medicinal
2010; 45: 4104-4112.
35. Masoumeh E, Mohammad K, Maryam FA. Coriandrum sativum evaluation of its anxiolytic 46. Millar AD, Rampton DS, Chander CL, Claxson AWD, Blades S, Coumbe A, Marris CJ, Blake D. Ethnopharmacol 2005; 96: 365-370.
Evaluating the antioxidant potential of new treatments for inflammatory bowel disease using 36. Pandey A, Bigoniya P, Raj V, Patel KK. rat model of colitis. Gut 1996; 39: 407-415.
Pharmacological screening of Coriandrum sativum Linn. for hepatoprotective activity. J 47. Hossam MM, Ramadan A, Hemeida, Ali IM, Pharm and Bioallied Sci July-September 2011; Farid MA. Prophylactic role of Curcumin in dextran sulphate sodium(DSS) induced ulcerative colitis murine model. Food and Chem 37. Fernanda CM, Claudia ML, Marina PA. Invitro Toxicol 2009; 47: 1311-1317.
effect of Aloe vera, Coriandrum sativum and Ricinus communis fractions on Leishmania 48. Saggu H, Cooksey J, Dexter DA (1989). infantum and on murine monocytic cells. Vet Selective increase in particular superoxide Parasitol 2011; 178: 235-240.
dismutase activity in parkinsonian subtansia
nigra. J. Neurochem.1989; 53: 692-697.
38. Al-Mofleha A, Alhaider AA, Mossa JS. Protection of gastric mucosal damage by 49. Beers JR, Sizer IW (1952). A spectrophotometric Coriandrum sativum L. pretreatment in Wistar method for measuring the breakdown of albino rats. Environ Toxicol Pharmacol 2006; 22:
hydrogen peroxide by catalase.J Biol Chem. 115:
39. Mansoor SA, Al-khamis KI, Mohammad WI. 50. Ellman GL. Tissue sulphydryl groups. Arch Post-coital antifertility activity of the seeds of Biochem Biophy 1959; 82: 70-77.
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013 51. Niehaus WG, Samuelsson B. Formation of 58. Loher F, Schmall K, Freytag P, Landauer N, Hallwachs R, Bauer C, Siegmund B, Rieder F, arachidonate during microsomal lipid Lehr HA, Dauer M, Kapp JF, Endres S, Eigler A. peroxidation. Eur J Biochem. 1968; 6: 126-130.
The specific type-4 phosphodiesterase inhibitor 52. Bradley PD, Friebal DA, Christensen RD. mesopram alleviates experimental colitis in Measurement of cutaneous inflammation : mice. J Pharmacol Exp Ther 2003; 305: 549-56.
estimation of neutrophil content with an enzyme 59. Keshavarzian A, Morgan G, Sedghi S, Gordon marker. J.Invest. Dermatol 1982; 78: 206-209.
JH, Doria M. Role of reactive oxygen 53. Lillie RD, Fullmer HM. Histopathologic metabolites in experimental colitis. Gut 1990; technique and practical histochemistry. New 31: 786-790.
York: Mc Graw-Hill 1976.
60. Keshavarzian A, Sedghi S, Kanofsky J. 54. Nakhai LA, Mohammadirad A, Yasa N, Minaie Excessive production of reactive oxygen B, Nikfar S, Ghazanfari G. Benefits of Zataria metabolites by inflamed colon. Analysis by multiflora Bioss in experimental model of mouse inflammatory bowel disease. Evid Based chemiluminescence probe. Gastroenterology Complement Alternat Med 2007; 4: 43-50.
1992; 103: 177-185.
55. Sharon P, Stenson WF. Metabolism of 61. Koutroubakis IE, Malliarki N, Dimoulios PD, arachidonic acid in acetic acid colitis in rats. Karmiris K, Castanas E, Kouroumalis EA. Gastroenterology 1985; 88: 55-63.
Decreased total and corrected antioxidant capacity in patients with inflammatory bowel 56. MacPherson B, Pfeiffer CJ. Experimental colitis. Digestion 1976; disease. Dig Dis Sci 2004; 14: 424-52.
57. Axelsson LG, Landstrom E, Bylund-Fellenius 62. Bobin-Dubigeon X, Collin N, Grimaud JM, AC. Experimental colitis induced by dextran Robert G, LeBaut L, Petit JY. Effect of tumor sulphate sodium in mice: beneficial effects of necrosis factor-á synthesis inhibitors on rat sulphasalazine and olsalazine. Aliment trinitrobenzene sulphonic acid-induced chronic Pharmacol Ther 1998; 12:925-934.
colitis. Eur J Pharmacol. 2001; 42: 103-110.
The Journal of Integrated Health Sciences Vol 1 Issue 2 December 2013


Multiple daily administrations of low-dosesublingual immunotherapy in allergicrhinoconjunctivitisVasco Bordignon, MD,* and Samuele E. Burastero, MD† Background: Sublingual immunotherapy (SLIT) is an efficacious treatment for allergic rhinoconjunctivitis.Objective: To investigate whether the number of daily administrations of SLIT can affect its efficacy.Methods: In an open study, 64 patients with allergic seasonal rhinoconjunctivitis to grass or birch pollens were assigned to

Das krankheitsbild

AUS KLINISCHER UND Petra Vetter Kontakt e-mail: [email protected] Inhalt Seite 2. Zur Begrifflichkeit.3 3. Probleme der diagnostischen Abklärung.4 3.1. Erklärungsansätze.4 3.2. Methoden.5 3.4. Conners Skala.5 4. Therapeutische Ansätze.6 4.1. Pädagogische Maßnahmen.6 4.2. Psychotherapien.6 4.3. Medikamentöse Behandlung.6