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甲基强的松龙对兔结肠炎模型中溃疡形成、基质金属蛋白酶分布及类花生酸生成的影响

Effect of methylprednisolone on the ulceration, matrix metalloproteinase distribution and eicosanoid production in a model of colitis in the rabbit.

作者信息

Anthony D, Savage F, Boulos P, Hembry R, Sams V, Trevethick M

机构信息

Department of Surgery, University College London Medical School, UK.

出版信息

Int J Exp Pathol. 1997 Dec;78(6):411-9. doi: 10.1046/j.1365-2613.1997.440373.x.

DOI:10.1046/j.1365-2613.1997.440373.x
PMID:9516873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2694554/
Abstract

This study has examined the response of a rabbit model of inflammatory bowel disease to methylprednisolone. Colitis was induced in the colon of rabbits with 40 mg trinitrobenzenesulphonic acid in 25% ethanol (TNBS). The effect of methylprednisolone (0.5 mg/kg/day) on the development of colitis was determined at one week, by examining the colon's macroscopic and microscopic appearance, the distribution of matrix metalloproteinases (MMPs) and by measuring eicosanoid production. Although there was no difference in the area of ulcerated colonic tissue in the treated and untreated TNBS animals, the increase in polymorphonuclear leucocytes was significantly reduced in TNBS rabbits given methylprednisolone. The only difference in the distribution of MMPs was a reduction in the number of polymorphonuclear leucocytes containing gelatinase B. The release of immunoreactive PGE2 and LTB4, but not 6-keto PGF1 alpha, was increased in the TNBS animals and was unchanged by methylprednisolone. These results show that methylprednisolone does not modify the injury produced by TNBS in this model despite reducing the infiltration of polymorphonuclear leucocytes. Hence it suggests that these cells do not contribute to the injury observed, are not the source of the eicosanoids and that gelatinase B is not required in the healing process in this model.

摘要

本研究检测了炎性肠病兔模型对甲泼尼龙的反应。用25%乙醇中的40mg三硝基苯磺酸(TNBS)诱导兔结肠发生结肠炎。通过检查结肠的大体和微观外观、基质金属蛋白酶(MMPs)的分布以及测量类花生酸的产生,在一周时确定甲泼尼龙(0.5mg/kg/天)对结肠炎发展的影响。尽管在接受治疗和未接受治疗的TNBS动物中,溃疡性结肠组织的面积没有差异,但给予甲泼尼龙的TNBS兔中多形核白细胞的增加显著减少。MMPs分布的唯一差异是含有明胶酶B的多形核白细胞数量减少。TNBS动物中免疫反应性PGE2和LTB4的释放增加,但6-酮PGF1α未增加,且甲泼尼龙对其无影响。这些结果表明,在该模型中,尽管甲泼尼龙减少了多形核白细胞的浸润,但并未改变TNBS所造成的损伤。因此,这表明这些细胞对所观察到的损伤没有作用,不是类花生酸的来源,并且在该模型的愈合过程中不需要明胶酶B。

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Macroscopic, microscopic and biochemical characterisation of spontaneous colitis in a transgenic mouse, deficient in the multiple drug resistance 1a gene.多药耐药1a基因缺陷型转基因小鼠自发性结肠炎的宏观、微观及生化特征
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Effects of a COX-2 preferential agent nimesulide on TNBS-induced acute inflammation in the gut.环氧化酶-2(COX-2)选择性药物尼美舒利对三硝基苯磺酸(TNBS)诱导的肠道急性炎症的影响。
Inflammation. 2001 Oct;25(5):301-10. doi: 10.1023/a:1012860509440.