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Histopathological Observation Of Dextran Sulfate Sodium Induced Ulcerative Colitis In Mice And The Distribution Of α-defensin4 Of In The Colon

Posted on:2010-08-22Degree:MasterType:Thesis
Country:ChinaCandidate:H WangFull Text:PDF
GTID:2143360278977629Subject:Basic veterinary science
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Ulcerative colitis (UC) is a chronic non-specific gastro-intestinal inflammation ,and the pathogenesis of its has not been clarified yet until now. In recent years, the incidence of ulcerative colitis has increased. UC which usually recurrent after treatment,has greatly affected the quality of patients'life, but also caused some serious complications even cancer. There is no effective treatment, which aroused researchers'great attention both at home and abroad in recent years to its etiopathogenisis and pathogenesis.In order to study the etiology and pathogenesis of UC,this experiment is according to the method of Cooper and has improved. 20 BALB / c mice were randomly divided into 2 groups, and the test group is drinked by Dextran sulfate sodium(DSS) of 7% seven days to induce UC of acute phase and the control group is drinked by distilled water. Parameters such as daily weight, stool and occult blood were observed and recorded,and the disease active index(DAI) score was carried out; With histopathological observation on crypt damage,inflammation,lesion depth and percent involvement, the histological index (HI) score was carried out; The model was evaluated by DAI and HI score.The results observe that BALB/c mice can occur diarrhea,bloody stool and there were the entire crypt disappeared, inflammatory cell infiltration in colon, after treated with 7% DSS solution for 7 days,HI and DAI score were in line with the Cooper standard, model was successful.In order to study the pathological changes of the model. In this study,we first observe the pathologic histology change of heart, liver, spleen, lungs, kidneys with routine paraffin section and HE staining.The results showed that epithelial cells was granular degeneration and the renal tubule was occlusion by the cytoplasm of epithelial cells in the renal proximal convoluted tubules liver cells was granular degeneration in the surrounding of lobules of liver, some liver cells had fatty degeneration. liver cells which was in the surrounding of central vein was cellular swelling.In lung, alveolar space appears asphyxial membrane and there was inflammation at pulmonary interstitial substance connective tissue medullary sinus was hyperemia in the peripheral of red pulp and white pulp of the spleen .myocardial cells was granular degeneration .The results showed that the DSS-UC model had extra-intestinal manifestations, and it was similar to human UC. This is not only conducive to awareness of DSS-UC model, but also to treatment of its extra-intestinal manifestations and early diagnosis of UC .It indicated that DSS-UC is a more satisfactory model of UC further.Defensins played an important role in the intestinal immune mechanisms.The changes and significance ofα-defensin4 in UC is reported raraly.To determine changes ofα-defensin4 in colonic mucosa of DSS-UC mouse model and explore whetherα-defensin4 is related to the pathogenesis of UC. Immunohistochemistry method was applied in this study and determined expression ofα-defensin4 in colonic mucosa of mouse model of DSS-UC. The primary antibody is goat-anti-mouse a-defensin-4 antibody and the secondary antibody is rabbit-anti-goat lgG with HRP labeled. The result shows that there are some positive pellets.in Paneth cells,epithelial goblet cells and enteric cavity of ileum.There weren't some positive pellets ofα-defensin4 in the intestinal gland but in enteric cavity of colon.the intestinal glands was loss in DSS-UC model of the colon,but there were some positive pellets ofα-defensin4 in around of relic intestinal glands, hyperplasia of the lamina propria connective tissue and the among of epithelial cells.It indicated thatα-defensin4 in the expression of DSS-induced colonic mucosa of mice was changed,α-defensin4 may be involved in the pathophysiological mechanism of occurrence of UC.
Keywords/Search Tags:DSS, BALB/c, UC, Histopathology, α-defensin-4
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