阿泰宁对牛结肠黏膜蛋白诱发大鼠免疫性溃疡性结肠炎的治疗作用  

Therapeutic effects of Ataining on immune ulcerative colitis induced by calf colonic mucosal protein in rats

作　　者：王文杰[1] 王霖[1] 刘洋[1] 彭珊瑛[1] 张弗盈[1] 李萍[1] 万阜昌 崔云龙 

机构地区：[1]中国医学科学院中国协和医科大学药物研究所,北京市100050 [2]青岛市微生态工程技术研究中心,山东省青岛市266400 [3]青岛东海药业有限公司,山东省青岛市266400

出　　处：《世界华人消化杂志》2008年第1期25-32,共8页World Chinese Journal of Digestology

基　　金：系列微生态生物新药高技术产业化示范工程项目资助;No.发改高技[2004]2078号~~

摘　　要：目的:观察阿泰宁对牛结肠黏膜蛋白(CCMP)诱发大鼠免疫性溃疡性结肠炎(UC)的治疗作用及机制.方法:将大鼠随机分为空白对照A组(n=8),模型B组(n=10),美沙拉秦(5-SAS)C组(n=10),阿泰宁大,小剂量D,E组(10^(11)CFU/L,10^(10)CFU/L),阿泰宁大剂量+美沙拉秦F组(n=10),21 d后处死动物.肉眼观察结肠病变,分别测体质量、结肠湿质量、溃疡指数和结肠组织病理学变化.用MTT法测定各组肠系膜T/B淋巴细胞转化率,ELISA法测定大鼠血清中IL-8和TNF-α含量,单向免疫扩散法测定血清样品中IgG含量.结果:B,C,D,E组大鼠体质量均小于A组,但没有显著性差异.B组大多数大鼠排出的便呈白色.黏液且质软,治疗后排便均正常,结肠病变均减轻.C、D、E组大鼠的肠湿质量指数和溃疡指数得分以及D、E和F组的结肠中上段肠黏膜病变积分与B组均显著降低.与B组相比.C、D、E和F组的T淋巴细胞转化率显著增高(1.53±0.44,1.25±0.49,1.39±0.40,1.18±0.41 vs 0.59±0.20,P<0.05).而血清中IL-8含量均显著降低(47.7±16.9 ng/L,39.7±13.4 ng/L,57.0±8.6 ng/L,31.9±5.0 ng/L vs 81.0±10.9 ng/L,P<0.01),D、E,F组血清中TNF-α和D,F组IgG的含量均显著降低(TNF-α:31.7±11.2 ng/L,47.2±21.7 ng/L,30.3±17.1 ng/L vs 78.0±12.3 ng/L;IgG:9.6±1.8 g/L,7.5±0.2 g/L vs 11.9±0.4 g/L,P<0.05).结论:用CCMP可使大鼠结肠黏膜出现典型UC病变,并伴随IL-8、TNF-α、IgG致炎因子显著升高,T淋巴细胞转化率显著减低.用阿泰宁治疗后,IL-8、TNF-α及IgG的表达下调,T淋巴细胞转化升高,肠黏膜溃疡被修复.阿泰宁和美沙拉秦有协同作用.AIM： To study the therapeutic effects of Ataining （Clostridium butyricum, CGMCC 0313.1 strain） on immune ulcerative colitis （UC） induced by calf colonic mucosal protein （CCMP） in rats. METHODS： Rats were randomly divided into： UC model ＋ saline （group B）, UC model ＋ C. butyricum （10^11 CFU/L） （group D）, UC model ＋C. butyricum （10^10 CFU/L） （group E）, UC model ＋ mesalazine （5-SAS, 200 g/L） （group C）, UC model ＋ C. butyricum （10^11 CFU/L） ＋ 5-SAS （100 g/L） （group F）, and non-UC model （group A）. After 21 d, all animals were killed by decollation. Colon mucosal damage was observed with the naked eyes. Body weight, colon wet weight, and ulcerative index were measured. Pathological changes in colon tissue were observed by microscopy. The conversion rate of T and B lymphocytes from intestinal mesentery was measured by MTT assay. Serum interleukin-8 （IL-8） and tumor necrosis factor-α （TNF-α） were determined by ELISA. Serum IgG was determined by unilateral immune diffusion. RESULTS： Rats with UC produced white mucous feces. After treatment, they all produced normal feces. Compared with group B, colon wet weight, pathological colon mucosal damage and pathological damage to the upper and middle regions of colon mucosa in groups C -F were significantly reduced. Conversion of T lymphocytes in C, D, E, F groups was significantly increased （1.53 ±0.44, 1.25 ± 0.49, 1.39 ±0.40, 1.18± 0.41 vs 0.59 ±0.20, P 〈 0.05）. The content of IL-8 in serum of groups C-F was significantly reduced （47.7 ± 16.9 ng/L, 39.7 ±13.4 ng/L, 57.0± 8.6 ng/L, 31.9 ±5.0 ng/L vs 81.0 ±10.9 ng/L, P 〈 0.01）, however, the decrease in group E was greater than that in group C. Serum TNF-α in groups D-F was significantly decreased （31.7 ±11.2 ng/L, 47.2 ±21.7 ng/L, 30.3 ± 17.1 ng/L vs 78.0 ± 12.3 ng/L）. Serum IgG in groups D and F was reduced （9.6 ±1.8 g/L, 7.5 ± 0.2 g/L vs 11.9 ± 0.4 g/L, P 〈 0.05）. CONCLUSION： A rat model of UC co

关 键 词：免疫性溃疡性结肠炎 阿泰宁 美沙拉秦 酪酸梭菌 

分 类 号：R574.62[医药卫生—消化系统]