Rainey J B
Ann R Coll Surg Engl. 1986 May;68(3):130-3.
Cogent epidemiological and experimental data implicate bile acids as endogenous co-carcinogens in colorectal cancer. A series of experiments was designed to test the ability of sodium deoxycholate (SDC) to promote intestinal hyperplasia and neoplasia in rats (n = 265). The intermediary role of faecal anaerobes was explored in animals receiving oral metronidazole. Intrarectal instillation of SDC trebled tumour yield in functioning large bowel and increased both crypt depth and crypt cell production rate. Metronidazole reduced this tumour promotion without affecting SDC-induced hyperplasia. By contrast, SDC was totally inactive in colon isolated as a Thiry-Vella fistula. Bile acids probably promote colorectal carcinogenesis by stimulating mucosal hyperplasia but only in the presence of faeces.
有力的流行病学和实验数据表明胆汁酸是结直肠癌的内源性共致癌物。设计了一系列实验来测试脱氧胆酸钠（SDC）促进大鼠（n = 265）肠道增生和肿瘤形成的能力。在接受口服甲硝唑的动物中探索了粪便厌氧菌的中介作用。直肠内滴注SDC使正常功能的大肠肿瘤发生率增加两倍，并增加了隐窝深度和隐窝细胞产生率。甲硝唑可减少这种肿瘤促进作用，而不影响SDC诱导的增生。相比之下，SDC在作为Thiry-Vella瘘分离的结肠中完全无活性。胆汁酸可能通过刺激粘膜增生来促进结直肠癌发生，但仅在有粪便存在的情况下。
