Beneficial effects of Foeniculum vulgare on ethanol-induced acute gastric mucosal injury in rats Beneficial effects of Foeniculum vulgare on ethanol-induced acute gastric mucosal injury in rats

Beneficial effects of Foeniculum vulgare on ethanol-induced acute gastric mucosal injury in rats

  • 期刊名字:世界胃肠病学杂志(英文版)
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  • 论文作者:Fatih Mehmet Birdane,Mustafa C
  • 作者单位:Department of Internal Medicine,Department of Chemistry (Biochemistry Division),Department of Pharmacology and Toxicolog
  • 更新时间:2020-10-22
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PO Box 2345, Beijing 100023, ChinaWorld Gastroenterol 2007 January 28: 13(4): 607-611World Journal of Gastroenterology ISSN 1007-932792007 The wjG Press. All rights reserved.Beneficial effects of Foeniculum vulgare on ethanol-inducedacute gastric mucosal injury in ratsFatih Mehmet Birdane, Mustafa Cemek, Yavuz Osman Birdane Ilhami Gulin, Mehmet Emin BuyukokurogluFatih Mehmet Birdane Department of Internal Medicine, 2007 The W)G Press. All rights reserved.Faculty of Veterinary Medicine, Afyon Kocatepe University,Afyon, TurkeyKey words: Foeniculum vulgare; Ethanol; Rat; UlcerMustafa Cemek, Department of Chemistry(BiochemistAntioxidantDivision), Faculty of Science and Arts, Afyon KocatepeUniversity, Afyon, TurkeyBirdane FM, Cemek M, Birdane YO, Gulgin I, BuyukokurogluYavuz Osman Birdane, Department of Pharmacology and ME. Beneficial effects of Foeniculum vulgare on ethanol-Toxicology, Faculty of Veterinary Medicine, Afyon KocatepeUniversity, Afyon, Turkeyinduced acute gastric mucosal injury in rats. world JIlhami Gulgin, Department of Chemistry, Faculty of Science andGastroenterol2007;13(4):607-611rts, Ataturk University, Erzurum, TurkeyFacultyofMedicineAfyonKocatenepartmentofPharmacologyhttp://www.wjgnet.com/1007-9327/13/607.aspCorrespondence to: Mehmet Emin Buyukokuroglu, Departmentof Pharmacology, Faculty of Medicine, Afyon KocatepeUniversity, Ali Cetinkaya Kampusu, Izmir yolu8 km TR-03200,Afyonkarahisar, Turkey. memin(@aku.edu. trINTRODUCTIONTelephone:+90-272-2140152Fax:+90272-2142060epic ulcer is a common disorder of the gastrointestinalReceived: 2006-05-25Accepted: 2006-12-15system and millions of people suffer from this diseasein the world. The medical cost of treating peptic ulcerand its complications amounts to billions of dollarsAbstractannually. The pathogenesis of peptic ulcer disease ismultifactorial, including chronically using non-steroidAIM: To examine the anti-ulcerogenic and antioxidant anti-inflammatory drugs, cigarette smoking, alcohol, andeffects of aqueous extracts of Foeniculum vulgare(FVE) reactive oxygen species(ROS). ROS are generated by cellson ethanol-induced gastric lesions in rats.in some physiological and pathological circumstances. Anyderangement between pro-oxidants and antioxidants, inMETHODS: FVE was administered by gavage at doses which pro-oxidants prevail is known as oxidative stress"of 75, 150 and 300 mg/kg, and famotidine was used at Insufficient antioxidant protection or excess productionthe dose of 20 mg/kg. Following a 60 min period, all the of ROS can result in this condition. RoS can react with allrats were given 1 mL of ethanol(80%)by gavage. One macromolecules, such as lipids, proteins, nucleic acids, andhour after the administration of ethanol, all groups were carbohydrates, particularly polyunsaturated fatty acids onsacrificed, and the gastric ulcer index was calculated;cell membranes. After the beginning of an initial reactionwhole blood malondialdehyde(MDA)and reduced with ROS, a continuing chain reaction is started and cellglutathioneO), serum nitrate, nitrite, ascorbic acid, injury and, ultimately, cell death occur 2). Peptic uleretinol and B-carotene levels were measured in all theis produced by the imbalance between gastroduodenalmucosal defense mechanisms and offensive factors. SomeRESULTS: It was found that pretreatment with FVEtudies have revealed that ROS and lipid peroxidationsignificantly reduced ethanol-induced gastric damage. are implicated in the pathogenesis of ethanol-inducedThis effect of VE was highest and statistically significant gastric lesions and gastrointestinal damage, and they2.81 VS 13.15+4.08, P< 0.001). Also, pretreatment prostaglandins,. Therefore, treatment with antioxidantssignificantly increased GSH, nitrite, nitrate, ascorbic acid,gastric mucosal damageretinol and B-carotene levels.Fell-known umbelliferousP中国煤化工 s have been used asCONCLUSION: FVE has clearly a protective effect tradiCNMHe and China. It isagainst ethanol-induced gastric mucosal lesion, and this natie Mediterranean areaeffect, at least in part depends upon the reduction in The seeds of this plant have been known to be able toactivitclimacteric syndrome, and increase libid.ms of femalelipid peroxidation and augmentation in the antioxidant regulate menstruation, alleviate the symptFVE also08ISSN 1007-9327 CN 14-1219/ World J Gastroenterol January 28, 2007 Volume 13 Number 4possesses emnenagague and galactagogue properties". It acid)], phenylendiamine, sodium azide, 2, 4-dinitrophehas been reported that FVE could be used in the pediatric nylhydrazine, ethanol, hexane, sodium nitrite, sodiumcolic and some respiratory disorders due to its anti- nitrate, sulfanilamide, N-(1-Naphthyl)ethylenediaminespasmodic effects.. Seeds of it are used in folk remedies dihydrochloride and vanadium(ml)chloride wereis natively found in North and West regions of Turkey. It reagents used in this study were of analytical grade andfor treatment of dysmenorrhea FVE (in Turkish"Rezene purchased from Sigma. All the other chemicals andis cultivated for the herb as a spice(Favouring salads)andmedicine in Turkey. Powders or tablets(0.5-1 g of seeds, Ulcer studyor its infusion forms(2%)are taken 2-3 times per day. As The anti-ulcerogenic effect of FVE was investigated witha medicinal plant, FVE has been used as an antispasmodic, the ethanol-induced ulcer model. On the first day of thecarminative, diuretic, lactation stimulant, and as dressings experiment, groups 1, 2 and 3 were administered withfor wounds in Turkish traditional medicine. It 75, 150 and 300 mg/kg FVE, group 4 was administeredcontains 1%0-3% of a volatile oil, which is composed of with 20 mg/kg famotidine, and group 5 was administered50%0-85% of anethole and about 20% of d-fenchone ,2,. with saline solution. All of drugs were administered byOther compunds present in FVE are d-a-pinene, d-a- gavage at the same volume (0.5 mL). Following a 60 minphellandrene, dipentene, methyl chavicol, feniculun, period, all the rats were given 1 mL of ethanol(80%)byldehyde, and anisicgavage. One hour after the administration of ethanol,The aim of this work was to assess the gastroprotective rats were injected with a high dose of ketamine(100 mg/activity of FVE in rat models of experimentally ethanol- kg), blood samples were taken by cardiac punctures, andinduced gastric lesions. In particular, we investigated the stomachs were removed and opened along the greatercffects of aqucous extracts of FVE on gross mucosal curvature and washed in physiological saline solution Forlesions in the stomach, glutathione(GSH), nitrite, measurement of the gross gastric mucosal lesions, freshlynitrate, ascorbic acid, retinol and B-carotene levels, and excised stomachs were laid flat and the mucosal lesionsanges in lipid peroxidation determined by measuring were traced on clear acetate paper. Gross mucosal lesionsmalondialdehyde(MDA)levels in the bloodwere recognised as hemorrhage or linear breaks(erosions)with damage to the mucosal surface. The area of stomachMATERIALS AND METHODStissue and gross lesions were approximately calculatedPlant materialby planimetry using a simple magnifier. The results weretranslated to the term of"total ulcer area/total gastriThe aerial parts of FVE were collected in June 2003 from area""and these were expressed as an ulcer index(%)Bursa. The plant was identified by the Department ofBotany of Science and Arts Faculty, Ataturk University, Biochemical analysisErzurum, Turkey, where a voucher specimen is keptFasting blood samples were drawn into heparin-free tubesduring routine blood sampling for biochemical analysisExtraction and preparation of test sampleser immediate centrifugation(1000 g for 10 min at 4Air-dried FVE was pulverized with a blender. Obtained the serum was stored in polystyrene plastic tubes at-70'Cplant material(230 g) was mixed with boiling distilled water until analysis. Whole blood was collected into heparinizedand stirred on the hot plate for 15 min. Subsequently, it tubes and whole blood MDA and GSH levels were studiedwas filtered over Whatman No 1 paper. Finally, the filtrate on the same day of admission.was frozen and lyophilized in a lyophilizator(Labconco,Whole blood MDA(as an important indicator ofFreezone 1L, USA)at a 5 umHg pressure and-50C (14.9 g). lipid peroxidation) levels were measured according to amethod of Jain et a/ The principle of the method wasAnimalsbased on the spectrophotometric measurement of theThirty-five Sprague-Dawley rats with a weight range color developed during the reaction of thiobarbituricof 190-225 g were used for the experimentation. The acid with MDA. Concentrations of thiobarbituric acidrats were fed with standard laboratory chow and water reactive substances(TBARS)were calculated by thebefore the experiment. Rats were divided into 5 equal absorbance coefficient of malondialdchyde-thiobarbituricgroups(n= 7)and housed in cages. Twenty-four acid complex and expressed as nmol/mL. Wholehours before the experiment, the rats were fasted and blood GSH concentrations were also measured by theallowed access to water ad libitum. The investigation was spectrophotometric method. The concentrations ofconducted in accordance with the Guide for the Care nitric oxide(nitrate and nitrite)were detected by thend Use of Laboratory Animals published by the US methods of Miranda et al. Nitrite and nitrate calibrationNational Institutes of Health(NIH Publication no 85-23, standards were prepared by diluting sodium nitrite andrevised 1996)and approval has been received from our sodium nitrate in pure water. After loading the plate withinstitutional Animal ethics Committee.中国煤化工 radium (I) chlorideCN MHGide(50μandN-(1Chemicals used in this investigation, GSH, thiobarbituric Naphthy) ethylenediamine dihydrochloride(50 HL). Theacid, phosphate buffer, butylated hydroxytoluene, Griess solutions may also be premixed immediately priortrichloroacetic acid, EDTA, [5,5-dithiobis-(2-nitrobenzoic to application to the plate. Nitrite mixed with Griessww教据Birdane FM et al. Antiulcer effect of FVE6091 Effects of aqueous extracts of Foe FvE and famotidineanol-induced gastric mucosal Injury in rats芒Effects of aqueous extracts of FvE and famotidine onlood MDA and GSH, and serum nitrite and nitrate levelsGroups(mean±SD)%)MDANitrite13.15±4.08mg/kg FVE+ Ethanol8Control( ethano)529±0.64446±31133±07455±26150 mg/kg FVE+ ethane75451±1.04887±25256±09881±27300 mg/kg FVE+ Ethanol418±281FVE Ethanol20 mg/kg Famotidine Ethanol868±2633405±035679±334273±05888±19300 mg/kg412±0.6·5134±311.64±0.5552±17FVE Ethanol20 mg/kg398±075168±32210±08682±21Famotidine Ethanolents forms a chromophore from the diazotization ofanilamide by acidic nitrite followed by coupling with P<0. 05, "P<0.01, p<0.001,Ds ethanol.bicyclic amines, such as N-1-(naphthyl) ethylenediamine.Sample blank values were obtained by substituting dilutingmedium for Griess reagent Nitrite was measured in asimilar manner except that samples and nitrite standardswere only exposed to Griess reagents. The absorbanceserum antioxldant vitamins levels(mean SD)in ratsat 540 nm was read to assess the total level of nitrite and gAscorbic Add B-Carotene Redncnitrate in all samples. Serum vitamin C(ascorbic acid(mg/dL) (ug/dL)level was determined after derivatization with 2. 4-dinitr Control (ethanol)8】士0.22609±1.5phenylhydrazine. The levels of B-carotene at 425 nm75 mg/kg FVE+ Ethanoland vitamin A (retinol) at 325 nm were detected after the150 mg/kg FVE+ Ethanol±21b300 mg/kg FVE+ Ethanol098±022876±186845*4085±022748±195879±46reaction of serum: ethanol: hexane at the ratio of 1: 1: 320mg/ kg Famotidine+ Ethanol09±0.32655±165857±36"p<0.05,P<0.01. us ethanolStatistical analysisAll values were expressed as mean t SD. Statisticanalyses of data were performed using a one-way analysis increased at doses of 150 and 300 mg/kg FVE and inof variance(ANOVA) and Tukey's posttest. A value of famotidine groups ( Table 2). Nitrite and nitrate levels inP<0.05 was considered statistically significant.serum were decreased in the ethanol administered group,while increased in the FVe groups. This increase wasRESULTSsignificant only in 75 and 150 mg/kg FVE groups, butnot in 300 mg/kg FVE or famotidine groups(Table 2)Ulcer studyAll doses of Fve and famotidine increased the serumUlcer indices(UI) are shown in Table 1. Per-oral ascorbic acid levels, whereas only 300 mg/kg of FVEadministration of 80% ethanol produced multiple mucosal induced a significant increase (Table 3). On the otherlesions in the rat stomach. Pre-treatment with FVE and hand, serum B-carotene and retinol levels in FVE groupsfamotidine were found to inhibit ethanol-induced gastric were higher than that of control, while the difference wasmucosal injury. This inhibitor effect of FvE was highest significant only in the 150 mg/kg FVE group(Table 3)and statistically significant in the 300 mg/kg group ander1 50 mg/kg of FVe groups, the inhibitor effects on DISCUSsIONethanol-induced gastric mucosal injury were similar to For a long time, peptic ulcer has been one of the importantfamotidine group, which were not significant statistically. causes of morbidities and mortalities. Several factors suchFamotidine also significantly inhibited ethanol-induced as increased vascular permeability, gastric motility andgastric lesions compared with the controlvagal activity, decreased gastric blood Alow and protectiveprostaglandin levels play an important role in gastric ulcerBiochemical ana小yspathogenesis. The treatment of peptic ulcers is still a bigMDA levels of whole blood are shown in Table 2. Thechallenge and development of new drugs is urgent. Thereadministration of ethanol increased the MDA level are a number of medicinal plants that have been shown toin whole blood. In contrast, pretreatment with FVe be effective against ulcer diseases in traditional mediciney.significantly decrased the MDa levels at doses of 150 and Becatmedicinal plants may300 mg/kg, compared with ethanol administered alone中国煤化工e6 potential drugsAdditionally, famotidine was found to prevent the rise in InN MHGbeen done to exploMDA levelnew ant-ullfrom natural resources. and antiulcerGSH level in whole blood was decreased in the ethanol- activity of a variety of chemical compounP. In contrast, GSH levelsmedicinal plants have been determined leads isolated fromwww.wignet.com610ISSN 1007-9327 CN 14-1219/R World J Gastroenterol January 28, 2007 Volume 13 Number 4Ethanol is a commonly used ulcerogenic agent and showed the presence of up to 8% volatile oil (includingwhen given by gavage to rats, it produces severe gastric about 85% of anethole, up to 5% of estragole, andhemorrhagic lesions. The mechanism of ethanol-induced fenchone), flavonoids(rutin, quercetin and kaempferolstric lesions is varied, including the depletion of gastric glycosides), coumarins(bergapten, imperatorinmucus content, damaged mucosal blood Aow and mucosal xanthotoxin and marmesin), sterols and sugars. These arecell injury. In addition, ethanol-induced gastric mucosal also present in oil of FVE, d-a-pinene, d-a-phellandrenedamage is associated with overproduction of free radicals, dipentene, methyl chavicol, anisic acid, anisaldehyde andwhich lead to an increased lipid peroxidation. Increase limonene>>. Previous studies proved that anetholein lipid peroxide content and oxygen-derived free radicals possesses significant antioxidant, anti-inflammatorresults in marked changes in cellular levels and causes and ulcer healing activity in experimental modelsmembrane damage, cell death, exfoliation and epithelial Additionally, flavonoids, sterols, tannins and coumarinserosion. Accumulation of activated neutrophils in the of some plants are also known to possess antiulcergastric mucosa may be a source of free radicals. Several activity 5. Therefore, the presence of flavonoids contentstudies revealed that some antioxidant drugs such as and other bioactive compounds in FVE may be associatedmelatonin and dantrolene have protective effects against with the ulcer preventing actionethanol-induced acute gastric injury in rats. Results ofIn conclusion our data show that fve has an obviousthe present study showed that all doses of FVe preventegastroprotective effect and antioxidant propertiesgastric tissue damage against ethanol-induced stress, only Although it is unclear about the exact mechanismficantiv Inighest dose group. Furthermore, FVE underlying these actions, the effects on acute gastricdecreased the lipid peroxidation and increased the nonlesions suggest a multifactorial mechanism, involvingenzymatic antioxidant. Antioxidative properties may, at the antioxidant properties of FVE. FVE may be a newleast partially, be one of the possible mechanisms by which alternative for clinical management of gastric ulcer diseasesFVE ameliorated the ethanol-induced gastric lesions.and/or an antioxidant against oxidative stress. FurtherGSH is a well-known antioxidant, which is usually studies are required to clarify the anti-ulcer and antioxidantpresent as the most abundant low-molecularthiol in actions of FVemost organisms. It has various functions in the defenseagainst oxidative stress and xenobiotic toxicity. It can actas an electron donor for glutathione peroxidase in animal REFERENCEScells, and also directly reacts with ROS. GSH is readily 1 Halliwell B, Gutteridge JMC. Free Radicals in Biology andoxidized to glutathione disulfide(GSSG) by glutathioneMedicine. New York: Oxford University Press, 1989eroxidase, as well as by the reaction with ros, which2 Kannan K, Jain SK. Oxidative stress and apoptosismay subsequently cause the reduction in GSH levelsPathophysiology 2000: 7: 153-163o,. 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Pharmacol Res 2002; 45:a crude hydroalcoholic extract and coumarin isolated from4214425Mikania laevigata Schultz Bip. Phytomedicine 2005: 12: 72-77s- Editor Liu Y L- Editor Zhu Lh E- Editor Lu w中国煤化工CNMHGwww

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