Kajiura K, Ohkusa T, Okayasu I
Second Department of Surgery, Tokyo Medical and Dental University School of Medicine, Japan.
Digestion. 1998;59(1):69-72. doi: 10.1159/000007469.
The possible role of fecal bile acids in colorectal carcinogenesis in ulcerative colitis has been reported. In this study, we investigated the relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine colitis induced by dextran sulfate sodium.
Colorectal neoplasia in experimental colitis was induced by dextran sulfate sodium subsequent to a single azoxymethane pretreatment. Fecal bile acids were analyzed by gas-liquid chromatography.
Multiple high-grade dysplasias (intramucosal adenocarcinoma) and inflammatory changes were seen in all mice administered dextran sulfate sodium and azoxymethane. Inflammatory changes were also observed in all mice given dextran sulfate sodium only, while neither tumor nor inflammatory changes were detected in any of the control mice. Significant increases in cholic acid were observed in the mice of the colorectal tumor and experimental colitis groups during the experimental period, while in the control mice, no significant changes in fecal bile acids were observed.
It is suggested that fecal cholic acid and colitis may be intimately related to the development of colorectal neoplasia in this experimental model of murine colitis as well as in ulcerative colitis.
已有报道称粪便胆汁酸在溃疡性结肠炎的结直肠癌发生过程中可能发挥作用。在本研究中，我们调查了在葡聚糖硫酸钠诱导的实验性小鼠结肠炎中粪便胆汁酸与结直肠肿瘤发生之间的关系。
在单次给予氧化偶氮甲烷预处理后，用葡聚糖硫酸钠诱导实验性结肠炎中的结直肠肿瘤形成。通过气液色谱法分析粪便胆汁酸。
在所有给予葡聚糖硫酸钠和氧化偶氮甲烷的小鼠中均可见多处高级别发育异常（黏膜内腺癌）和炎症变化。仅给予葡聚糖硫酸钠的所有小鼠中也观察到炎症变化，而在任何对照小鼠中均未检测到肿瘤或炎症变化。在实验期间，结直肠肿瘤组和实验性结肠炎组小鼠的胆酸显著增加，而对照小鼠的粪便胆汁酸未观察到显著变化。
提示在该小鼠结肠炎实验模型以及溃疡性结肠炎中，粪便胆酸和结肠炎可能与结直肠肿瘤的发生密切相关。
