Meijers M, van Garderen-Hoetmer A, Lamers C B, Rovati L C, Jansen J B, Woutersen R A
Department of Biological Toxicology, TNO-CIVO Toxicology and Nutrition Institute, Zeist, The Netherlands.
Carcinogenesis. 1990 Dec;11(12):2223-6. doi: 10.1093/carcin/11.12.2223.
Cholecystokinin (CCK) has been shown to promote pancreatic growth and azaserine-induced pancreatic carcinogenesis in rats. The present study was carried out to determine effects of CCK on pancreatic growth and carcinogenesis in the N-nitrosobis(2-oxopropyl)amine (BOP) hamster model. One hundred male Syrian golden hamsters were injected s.c. once weekly with 20 mg BOP/kg body wt at 6, 7 and 8 weeks of age, and divided into four groups of 25 animals each, which received one of the following treatments (once daily, 3 days/week for 16 weeks): gelatin; CR-1409, a potent CCK-receptor antagonist; CCK-8, 2.5 micrograms/kg body wt; or CCK-8 in combination with CR-1409 (30 min before CCK treatment). The animals were killed after 19 weeks. The growth of the pancreas but not the incidence of pancreatic (pre)neoplastic lesions was enhanced by CCK-8. CR-1409 did not influence the effect of CCK on pancreatic growth.
胆囊收缩素(CCK)已被证明可促进大鼠胰腺生长及氮杂丝氨酸诱导的胰腺癌发生。本研究旨在确定CCK对N-亚硝基双(2-氧代丙基)胺(BOP)仓鼠模型中胰腺生长和癌变的影响。100只雄性叙利亚金仓鼠在6、7和8周龄时每周皮下注射一次20 mg BOP/kg体重,然后分为四组,每组25只动物,分别接受以下治疗之一(每天一次,每周3天,共16周):明胶;强效CCK受体拮抗剂CR-1409;2.5微克/千克体重的CCK-8;或CCK-8与CR-1409联合使用(在CCK治疗前30分钟)。19周后处死动物。CCK-8可促进胰腺生长,但不影响胰腺(癌)前病变的发生率。CR-1409不影响CCK对胰腺生长的作用。