熊去氧胆酸对三硝基苯磺酸诱导的结肠炎黏膜损伤的有益作用。

Beneficial effect of ursodeoxycholic acid on mucosal damage in trinitrobenzene sulphonic acid-induced colitis.

作者信息

Kullmann F, Arndt H, Gross V, Rüschoff J, Schölmerich J

机构信息

Department of Internal Medicine, University of Regensburg, Germany.

出版信息

Eur J Gastroenterol Hepatol. 1997 Dec;9(12):1205-11.

PMID:9471027

Abstract

BACKGROUND

Recently we observed that ursodeoxycholic acid (UDCA) ameliorates an experimental small intestinal inflammation induced by indomethacin in the rat. In this study, we have tested whether ursodeoxycholic acid also reduces mucosal damage in the bile-independent trinitrobenzene sulphonic acid (TNB) model of experimental colitis.

METHODS

Intestinal inflammation (colitis) was induced in male Sprague-Dawley rats (250-300 g) by intracolonic administration of TNB (30 mg in 50% ethanol). Rats were treated with UDCA (10 mg/kg) either for 3 days starting with the administration of TNB for an acute inflammation (n = 11) or for 8 days starting one day after induction of colitis related to a more acute/chronic inflammation (n = 11). Rats were sacrificed at day 3 or day 9, respectively. Healing of induced colitis was assessed by macroscopic and blinded microscopic analysis as well as by measurement of bowel wet weight, daily body weight, and myeloperoxidase activity. All examinations were separately performed in three colon segments (S1 3-5 cm, S2 5.5-8 cm and S3 8.5-11 cm from anus).

RESULTS

UDCA treatment significantly reduced macroscopically and microscopically detectable injury in acute inflammation in segments 1 and 2. The colitis-rats with acute/chronic inflammation had less marked mucosal damage. Nevertheless, UDCA treatment led to a significant decrease of visible injury parameters which was seen exclusively at the area of maximal ulceration (S2). Furthermore, a significant increase in body weight of UDCA-treated TNB rats compared to controls from day 5 on was found.

CONCLUSION

Ursodeoxycholic acid attenuates the severity of acute inflammation and inhibits the development of acute/chronic inflammation predominantly around the area of maximal ulceration in TNB-induced colitis. In addition to our previous studies and results in indomethacin induced enteritis, these data may provide a rationale for studying how UDCA modulates functions of immune cells in the colonic mucosa.

摘要

背景

最近我们观察到熊去氧胆酸（UDCA）可改善吲哚美辛诱导的大鼠实验性小肠炎症。在本研究中，我们测试了熊去氧胆酸是否也能减轻胆汁非依赖性三硝基苯磺酸（TNB）实验性结肠炎模型中的黏膜损伤。

方法

通过结肠内注射TNB（30mg溶于50%乙醇）诱导雄性Sprague-Dawley大鼠（250-300g）发生肠道炎症（结肠炎）。UDCA（10mg/kg）治疗大鼠，对于急性炎症，从注射TNB开始持续3天（n = 11）；对于与更急性/慢性炎症相关的结肠炎，在诱导结肠炎1天后开始持续8天（n = 11）。分别在第3天或第9天处死大鼠。通过宏观和盲法显微镜分析以及测量肠湿重、每日体重和髓过氧化物酶活性来评估诱导性结肠炎的愈合情况。所有检查分别在三个结肠段（距肛门S1 3-5cm、S2 5.5-8cm和S3 8.5-11cm）进行。