Tasi Y, Baba N, Nishimura I, Manabe T, Tobe T
Department of Surgery, Shiga Adult Disease Center.
Nihon Shokakibyo Gakkai Zasshi. 1991 Apr;88(4):1097-104.
The effects of CR1505, a CCK antagonist, on CCK-stimulated and normal pancreas were studied in Syrian golden hamsters. The CCK-stimulated trophic effect was inhibited by CR1505 in a dose-dependent manner, in which CR1505 100 mg/kg bw resulted in a complete inhibition of the weight of pancreas, the total pancreatic protein and DNA contents, compared to the control. Otherwise, CR1505 administration in doses of 25, 50, 100 mg/kg bw alone, didn't induce any significant changes among CR1505-treated groups and the control one. However, in the dose of 200 mg/kg bw, the weight of pancreas, the total pancreatic protein and DNA contents were significantly lower than control levels, suggesting pancreatic atrophy in the hamster. It's concluded that CR1505 is an effective CCK receptor antagonist that could inhibit the CCK-induced pancreatic trophic effect. Furthermore, CR1505 administration to normal pancreas brought out pancreatic atrophy, indicating that CCK seems to play an important role in the maintenance of normal pancreatic growth in hamsters.
在叙利亚金仓鼠中研究了CCK拮抗剂CR1505对CCK刺激的胰腺和正常胰腺的影响。CR1505以剂量依赖性方式抑制CCK刺激的营养作用,其中与对照组相比,100mg/kg体重的CR1505导致胰腺重量、胰腺总蛋白和DNA含量完全受到抑制。否则,单独给予25、50、100mg/kg体重剂量的CR1505,在CR1505处理组和对照组之间未引起任何显著变化。然而,在200mg/kg体重剂量下,胰腺重量、胰腺总蛋白和DNA含量显著低于对照水平,表明仓鼠出现胰腺萎缩。结论是CR1505是一种有效的CCK受体拮抗剂,可抑制CCK诱导的胰腺营养作用。此外,对正常胰腺给予CR1505会导致胰腺萎缩,表明CCK似乎在维持仓鼠正常胰腺生长中起重要作用。