Pour P M, Donnelly T, Stepan K
Am J Pathol. 1983 Aug;112(2):178-84.
Experiments were designed to investigate in the hamster model the effect on pancreatic carcinogenesis of bethanechol chloride (BC), which is known to increase pancreatic protein synthesis in rats. Hamsters received a single (15 mg/kg body weight) dose of BC either before, simultaneously with, or after a single dose of N-nitrosobis(2-oxopropyl)amine (BOP; 20 mg/kg body weight). A second group was treated daily with BC (7.5 mg/kg body weight) for 24 weeks, following BOP. The control groups consisted of animals treated with BOP only, with BC only, and with solvent only. The surviving hamsters were killed 46 weeks after BOP treatment. BC, whether given before, simultaneously with, or after BOP, significantly reduced the incidence of pancreatic ductal/ductular carcinomas. The multiplicity, size, and latency of carcinomas were also affected by BC. A more pronounced inhibition of cancer induction occurred in the group treated daily with BC after BOP. The possible mechanisms involved in the inhibitory action of BC on pancreatic carcinogenesis are discussed.
开展实验以在仓鼠模型中研究氯化氨甲酰甲胆碱(BC)对胰腺癌发生的影响,已知BC可增加大鼠胰腺蛋白质合成。仓鼠在单次给予N-亚硝基双(2-氧代丙基)胺(BOP;20mg/kg体重)之前、同时或之后,接受单次剂量的BC(15mg/kg体重)。第二组在给予BOP后,每日用BC(7.5mg/kg体重)治疗24周。对照组包括仅用BOP治疗、仅用BC治疗和仅用溶剂治疗的动物。在BOP治疗46周后,处死存活的仓鼠。BC无论在BOP之前、同时还是之后给予,均显著降低胰腺导管/小导管癌的发生率。癌的数量、大小和潜伏期也受到BC的影响。在BOP后每日用BC治疗的组中,对癌症诱导的抑制作用更为明显。讨论了BC对胰腺癌发生抑制作用的可能机制。