KCI등재후보
흰쥐에서 TNBS 로 유발된 염중성대장염의 병태생리에 관한 연구 = The Pathophysiology of Inflammatory Bowel Disease Induced by TNBS in Rat
저자
김나영(Na Young Kim) ; 김재준(Jae Jun Kim) ; 송인성(In Sung Song) ; 김정룡(Chung Yong Kim) ; 김우호(Woo Ho Kim)
발행기관
학술지명
권호사항
발행연도
1994
작성언어
-주제어
KDC
500
등재정보
KCI등재후보
자료형태
학술저널
발행기관 URL
수록면
20-35(16쪽)
제공처
소장기관
Objectives: The etiology and pathogenesis of ulcerative colitis and Crohn's disease(inflammatory bowel disease (IBD)) are still unknown although intensive research has been carried out in this area. A major limitation to this area has been the relative paucity of relevant animal models. The aims of this study are, first to establish the appropriate animal model for studying for IBD, and second to find out the chemical mediators involving the pathophysiology of IBD. Method: In the first study for establishing an animal model of IBD, 1 ml of 4% acetic acid was instilled into the lumen of the colon of 8 rats, and 1.2 ml of trinitrobenzene sulfonic acid (TNBS, 25 mg/ml) m 50%(v/v) ethanol was instilled into the lumen of the colon of the 16 rats; on the other hand, 1.2 ml of phosphate buffered saline (PBS) was instilled into the lumen of the colon of the 4 control rats. The gross and microscopic finding of the colon was observed 4Shrs, 1wk, 2wks, 4wks later after the instillation of each material. In the second study, PG₂, LTB₄ and specific activities of superoxide dismutase (SOD), catalase, xanthine oxidase were measured in the colon mucosa of 29 rats 48hrs, 2wks, 4wks after the instillation of 1.2 ml of TNBS (25 mg/ml) in 50% ethanol (v/v), and in the mucosa of 10 control rats 4wks after the instillation of 1.2 ml of FBS. Results: 1) In the first study the gross finding of the control group was all normal, and the acetic acid group showed mild focal hyperemia in 48hrs, 1wk, 2wks after instillation. On the other hand, the TNBS group of 48hrs showed black necrosis up to 7 cm from the anal verge in all 4 rats, in the TNBS group of 1wk, 1-1.5 cm sized active ulcerations, in the group of 2wks, 0.2-1 cm sized shallow ulcerations were scattered, and in the group of 4wks, healing to scar stage ulcerations were found. 2) The microscapic finding of the control group was all normal, and the 4% acetic acid group of 48hrs and 1wk showed infiltration of acute inflammatory cells; all rats of 48hrs and 1wk groups showed infiltration of acute inflammatory cells; all rats of 2wk and 4wk groups showed normal finding except mucosal ulceration in the one rat of two after 2wks. On the other hand, all of the 4 rats of 48hr TNBS group showed very severe acute inflammation, which resolved with appearance of chronic inflammation around the deep ulcer in 1wk later. Two weeks later, chronic inflammation became prominent, and 4wks later, chronic inflammation further progressed with fibrosis. 3) In the second study for studying pathophysiology of IBD caused by TNBS, the mean PGE₂ level of the control group was 289.9 pg/mg mucosa, and that of 4Shr TNBS group was 382.2 pg/mg mucosa without statistical significance. The mean PGE₂ level of 2wk and 4wk TNBS groups were 650.4 pg/mg mucosa and 710.4 pg/ mg mucosa, respectively, which were significantly higher than that of the control group. 4) The mean LTB₄ level of the control group was 4.4 pg/mg mucosa, and those of 48hr, 2wk, 4wk TNBS groups were 44.6 pg/mg mucosa, 106.6 pg/mg mucosa, and 52.8 pg/mg mucosa, respectively, which were all significantly higher than that of the control group. 5) The Cu, Zn SOD activity of the 48hr TNBS group was 0.47 unit/mg protein and this was significantly lower than that of control group, 9.37 unit/mg protein. Those of 2wk and 4wk TNBS groups were 1.84 unit/mg protein and 5.85 unit/mg protein, respectively. The Mn SOD activity of contro1 group was 0.79 unit/mg protein, and that of 48hr TNBS group was 0.57 unit/mg protein without statistical significance. However, those of 2wk and 4wk TNBS groups were 5.58 unit/mg protein and 3.69 unit/mg protein, respectively, which were significantly higher than that of the control group. 6) The catalase activity of the 4Shr TNBS group was 1.32 unit/mg protein and this was significantly lower than that of control group, 2.95 unit/mg protein. Those of 2wk and 4wk TNBS groups were 2.08 unit/mg protein and 2.52 unit/mg protein, and they had no
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