Slomiany B L, Piotrowski J, Slomiany A
Research Center, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, 07103-2400, USA.
Biochem Biophys Res Commun. 2000 Jan 27;267(3):801-5. doi: 10.1006/bbrc.1999.2037.
Endothelin-1 (ET-1) is a vasoactive peptide produced from a biologically inactive big ET-1 by the action of endothelin-converting enzyme-1 (ECE-1). We investigated gastric mucosal expression of ECE-1 during a 10-day course of inflammatory responses associated with acute gastritis elicited by Helicobacter pylori lipopolysaccharide. The ECE-1 activity was associated with microsomal fraction and the level of its expression reflected the extent of mucosal inflammatory involvement. The histologic pattern of inflammation reached a maximum on the 4th day following the lipopolysaccharide and was accompanied by a 4.1-fold enhancement in the expression of ECE-1 activity and a significant elevation in ET-1 (3.1-fold), TNF-alpha (8.8-fold), and apoptosis (11.6-fold). A 41.5% decrease in the severity of mucosal inflammation by the 10th day following the lipopolysaccharide was reflected in a 62.3% reduction in the mucosal expression of ECE-1 and a decline in TNF-alpha, ET-1, and apoptosis. Thus, H. pylori infection causes up-regulation of gastric mucosal ECE-1 expression, which leads to the enhancement of ET-1 production, induction of TNF-alpha, and triggering the apoptotic events that exacerbate the inflammatory process.
内皮素 -1（ET -1）是一种血管活性肽，由生物活性不高的大内皮素 -1在内皮素转换酶 -1（ECE -1）的作用下产生。我们研究了幽门螺杆菌脂多糖引发的急性胃炎相关炎症反应的10天病程中胃黏膜ECE -1的表达情况。ECE -1活性与微粒体部分相关，其表达水平反映了黏膜炎症累及的程度。脂多糖注射后第4天炎症组织学模式达到峰值，同时ECE -1活性表达增强4.1倍，ET -1（3.1倍）、肿瘤坏死因子 -α（TNF -α，8.8倍）和细胞凋亡（11.6倍）显著升高。脂多糖注射后第10天，黏膜炎症严重程度降低41.5%，这反映在黏膜ECE -1表达降低62.3%，以及TNF -α、ET -1和细胞凋亡的下降。因此，幽门螺杆菌感染导致胃黏膜ECE -1表达上调，进而导致ET -1生成增加、TNF -α诱导以及引发加剧炎症过程的凋亡事件。
