Sharon P, Ligumsky M, Rachmilewitz D, Zor U
Gastroenterology. 1978 Oct;75(4):638-40.
Prostaglandin E2 (PGE2) level in rectal mucosa excised from 17 patients suffering from ulcerative colitis was 2-fold higher than that found in rectal mucosa of 17 normal subjects: 2.0 +/- 0.4 and 0.9 +/- 0.2 ng per mg of wet tissue, respectively. Accumulation of PGE 2 in 24-hr cultures of rectal mucosa specimens obtained from patients with ulcerative colitis was 112% higher than that observed in cultures from control subjects. Addition of sulfasalazine, sulfapyridine, and 5-aminosalicylic, acid to the culture medium of ulcerative colitis mucosa resulted in inhibition of PGE2 production by 34, 32, and 62%, respectively, compared to rectal specimens cultured in drug-free medium. These results suggest that PGE may mediate the inflammatory response in ulcerative colitis and that some of the therapeutic effect of sulfasalazine and its constituents are related to the inhibition of PGE synthesis.
从17例溃疡性结肠炎患者切除的直肠黏膜中前列腺素E2(PGE2)水平比17例正常受试者直肠黏膜中的水平高2倍,分别为每毫克湿组织2.0±0.4纳克和0.9±0.2纳克。溃疡性结肠炎患者直肠黏膜标本在24小时培养中PGE2的积累比对照受试者培养中观察到的高112%。与在无药物培养基中培养的直肠标本相比,向溃疡性结肠炎黏膜培养基中添加柳氮磺胺吡啶、磺胺吡啶和5-氨基水杨酸分别导致PGE2产生抑制34%、32%和62%。这些结果表明,PGE可能介导溃疡性结肠炎中的炎症反应,柳氮磺胺吡啶及其成分的一些治疗作用与PGE合成的抑制有关。