Liu Xiao-chang, Mei Qiao, Xu Jian-ming, Hu Jing
Department of Gastroenterology, The First Affiliated Hospital, Anhui Medical University, Hefei 230032,China.
Zhonghua Wei Chang Wai Ke Za Zhi. 2009 Mar;12(2):193-6.
To investigate the effect of balsalazide on intestinal mucosal permeability of experimental colitis induced by dextran sulfate sodium(DSS) in a mouse model and its possible mechanism.
Forty-five C57BL/6J mice were randomly divided into five groups. Normal group was only fed with distilled water, DSS group and Balsalazide groups at doses of 42,141,423 mg/kg were fed with 5% DSS. Balsalazide was given by intragastric administration. DAI was evaluated daily. At the end of the experiment, colon tissue was collected for assessment of histological changes, MDA content, MPO, SOD and GSH-PX activity. Small intestinal mucosa was collected for assessment of transmission electron microscope(TEM), and detection of permeability by Evans blue.
Compared with normal group, DSS group mice all manifested severe weight loss associated with hematochezia and diarrhea with significant increase of DAI and HI score(P<0.01). MDA content and MPO activity was increased with the reverse result of SOD and GSH-PX(P<0.01) in DSS group. Intestinal mucosa showed a focal reduction in thinning of microvillous carpet and even a total disarrangement of epithelial surface, with decurtated and broaden junctional complex and enlarged intercellular space under TEM observations in DSS group. The amount of Evans blue permeated into intestinal wall was obvious in DSS group. Compared with DSS group, balsalazide improved gross findings, decreased MPO activity and MDA content, but increased the activity of SOD and GSH-PX(P<0.05). The amount of Evans blue permeated into intestinal wall was less(P<0.05). Ileal microvillous carpet was ameliorated in dose-dependent manner by balsalazide.
Intestinal mucosal permeability is increased in DSS group. Balsalazide can significantly ameliorate intestinal mucosal permeability in colitis model.
研究巴柳氮对葡聚糖硫酸钠（DSS）诱导的小鼠实验性结肠炎肠黏膜通透性的影响及其可能机制。
将45只C57BL/6J小鼠随机分为5组。正常组仅给予蒸馏水，DSS组及剂量为42、141、423mg/kg的巴柳氮组给予5% DSS。巴柳氮通过灌胃给药。每日评估疾病活动指数（DAI）。实验结束时，收集结肠组织评估组织学变化、丙二醛（MDA）含量、髓过氧化物酶（MPO）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-PX）活性。收集小肠黏膜进行透射电子显微镜（TEM）评估，并通过伊文思蓝检测通透性。
与正常组相比，DSS组小鼠均出现严重体重减轻，伴有便血和腹泻，DAI和组织学损伤（HI）评分显著增加（P<0.01）。DSS组MDA含量和MPO活性增加，SOD和GSH-PX活性则相反（P<0.01）。TEM观察显示，DSS组肠黏膜微绒毛毯局部变薄甚至上皮表面完全紊乱，连接复合体缩短变宽，细胞间隙增大。DSS组伊文思蓝渗入肠壁的量明显增加。与DSS组相比，巴柳氮改善了大体表现，降低了MPO活性和MDA含量，但增加了SOD和GSH-PX活性（P<0.05）。伊文思蓝渗入肠壁的量减少（P<0.05）。巴柳氮以剂量依赖方式改善回肠微绒毛毯。
DSS组肠黏膜通透性增加。巴柳氮可显著改善结肠炎模型的肠黏膜通透性。
