Fitzpatrick Leo R, Jenabzadeh Paniz
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, California Northstate University, Elk Grove, CA, United States.
Front Physiol. 2020 Jun 12;11:564. doi: 10.3389/fphys.2020.00564. eCollection 2020.
Inflammatory bowel disease (IBD) causes chronic inflammation affecting the GI tract. It is classified as consisting of Crohn's Disease (CD) and Ulcerative Colitis (UC). Bile Acid absorption is altered in both pre-clinical models of Inflammatory Bowel Disease (IB) and in human IBD. The bile acid transporter apical sodium dependent bile acid transporter (ASBT) showed decreased expression in rats with TNBS colitis. Decreased ASBT expression has also been described in murine, canine and rabbit models of intestinal inflammation. Human IBD studies have shown that an inflamed ileum can interrupt enterohepatic recirculation of bile acid, which could be due to inflammatory cytokine induced repression of the ASBT promoter. There are different hypotheses as to why ASBT is downregulated during CD. In addition, one study has demonstrated the beneficial effect of a glucocorticoid on ASBT expression, when treating IBD. Our aim in this paper was to systematically review various aspects of bile acid malabsorption in animal models of intestinal inflammation, as well as in IBD.
炎症性肠病（IBD）会引发影响胃肠道的慢性炎症。它被分类为由克罗恩病（CD）和溃疡性结肠炎（UC）组成。在炎症性肠病（IB）的临床前模型以及人类IBD中，胆汁酸吸收均发生改变。胆汁酸转运体顶端钠依赖性胆汁酸转运体（ASBT）在患有三硝基苯磺酸（TNBS）结肠炎的大鼠中表达降低。在肠道炎症的小鼠、犬和兔模型中也描述了ASBT表达降低的情况。人类IBD研究表明，发炎的回肠会中断胆汁酸的肠肝循环，这可能是由于炎性细胞因子诱导ASBT启动子的抑制。关于在克罗恩病期间ASBT下调的原因有不同的假说。此外，一项研究表明，在治疗IBD时，糖皮质激素对ASBT表达有有益作用。本文的目的是系统评价肠道炎症动物模型以及IBD中胆汁酸吸收不良的各个方面。
