Pour P M, Lawson T, Helgeson S, Donnelly T, Stepan K
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha 68105.
Carcinogenesis. 1988 Apr;9(4):597-601. doi: 10.1093/carcin/9.4.597.
To examine the effect of cholecystokinin (CCK) on pancreatic carcinogenicity in the hamster model, two sets of experiments were carried out. In one study, CCK (20 IDU/kg body wt) was given 3 h before, simultaneously with or 3 h after a single dose (20 mg/kg body wt) of N-nitrosobis(2-oxopropyl)amine (BOP). In another experiment, hamsters were treated similarly except that both CCK (20 IDU/kg body wt) and BOP (2.5 mg/kg body wt) were given weekly for 20 weeks. The results showed that CCK in the first experiment (single BOP dose) inhibited pancreatic cancer induction in a statistically significant fashion when given either 3 h prior to (P less than 0.05) or simultaneously with BOP (P less than 0.0005); however, CCK, when administered after BOP did not alter the cancer incidence as compared with hamsters treated with BOP alone. In the second experiment (chronic BOP treatment) the pattern and the incidence of pancreatic tumors were not affected by CCK.
为研究胆囊收缩素(CCK)对仓鼠模型胰腺癌发生的影响,进行了两组实验。在一项研究中,在给予单剂量(20毫克/千克体重)的N-亚硝基双(2-氧代丙基)胺(BOP)前3小时、同时或后3小时给予CCK(20国际单位/千克体重)。在另一项实验中,仓鼠接受类似处理,不同的是CCK(20国际单位/千克体重)和BOP(2.5毫克/千克体重)每周给药一次,共20周。结果显示,在第一个实验(单次BOP剂量)中,当在BOP前3小时(P<0.05)或与BOP同时给药时(P<0.0005),CCK以统计学显著方式抑制胰腺癌的诱发;然而,与仅用BOP处理的仓鼠相比,在BOP后给予CCK并没有改变癌症发生率。在第二个实验(慢性BOP处理)中,胰腺肿瘤的模式和发生率不受CCK影响。