Singer I I, Kawka D W, Schloemann S, Tessner T, Riehl T, Stenson W F
Department of Inflammation Research, Merck Research Laboratories, Rahway, New Jersey, USA.
Gastroenterology. 1998 Aug;115(2):297-306. doi: 10.1016/s0016-5085(98)70196-9.
BACKGROUND & AIMS: Prostaglandins are synthesized by cyclooxygenases (COX)-1 and -2. The expression and cellular localization of COX-1 and COX-2 in normal human colon and inflammatory bowel disease (IBD) surgical resections were studied.
COX-1 and COX-2 protein expression and cellular localization were assessed by Western blotting and immunohistochemistry.
COX-1 protein was expressed at equal levels in normal, Crohn's disease, and ulcerative colitis colonic epithelial cells. COX-2 protein was not detected in normal epithelial cells but was detected in Crohn's disease and ulcerative colitis epithelial cells. Immunohistochemistry of normal, Crohn's colitis, and ulcerative colitis tissue showed equivalent COX-1 expression in epithelial cells in the lower half of the colonic crypts. COX-2 expression was absent from normal colon, whereas in Crohn's colitis and ulcerative colitis, COX-2 was observed in apical epithelial cells and in lamina propria mononuclear cells. In Crohn's ileitis, COX-2 was present in the villus epithelial cells. In ulcerative colitis, colonic epithelial cells expressing COX-2 also expressed inducible nitric oxide synthase.
COX-1 was localized in the crypt epithelium of the normal ileum and colon, and its expression was unchanged in IBD. COX-2 was undetectable in normal ileum or colon, but it was induced in apical epithelial cells of inflamed foci in IBD.
前列腺素由环氧化酶(COX)-1和-2合成。研究了COX-1和COX-2在正常人类结肠及炎症性肠病(IBD)手术切除组织中的表达及细胞定位。
通过蛋白质免疫印迹法和免疫组织化学法评估COX-1和COX-2蛋白的表达及细胞定位。
COX-1蛋白在正常、克罗恩病及溃疡性结肠炎的结肠上皮细胞中表达水平相同。正常上皮细胞中未检测到COX-2蛋白,但在克罗恩病和溃疡性结肠炎的上皮细胞中可检测到。正常、克罗恩结肠炎及溃疡性结肠炎组织的免疫组织化学显示,结肠隐窝下半部的上皮细胞中COX-1表达相当。正常结肠中不存在COX-2表达,而在克罗恩结肠炎和溃疡性结肠炎中,COX-2在上皮细胞顶端及固有层单核细胞中可见。在克罗恩回肠炎中,COX-2存在于绒毛上皮细胞中。在溃疡性结肠炎中,表达COX-2的结肠上皮细胞也表达诱导型一氧化氮合酶。
COX-1定位于正常回肠和结肠的隐窝上皮,其在IBD中的表达无变化。正常回肠或结肠中未检测到COX-2,但在IBD炎症灶的顶端上皮细胞中可诱导其表达。