Inhibitory effects of protocatechuic acid on the post-initiation phase of hamster pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine.
Inhibitory effects of protocatechuic acid on the post-initiation phase of hamster pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine.
复制标题
原儿茶酸对 N-亚硝基双（2-氧代丙基）胺诱导的仓鼠胰腺癌发生后起始阶段的抑制作用。
作者：
H. Nakamura;A. Nishikawa;F. Furukawa;K. Kasahara;M. Miyauchi;H. Son;M. Hirose
本实验观察了原儿茶酸（PCA）对N-亚硝基双（2-氧代丙基）胺（BOP）诱发的仓鼠胰腺肿瘤发生的后诱发阶段的化学预防作用。将5周龄雌性仓鼠分为6组。第1-3组中的动物，每组由30只仓鼠组成，注射20 mg/kg体重的BOP，间隔一周作为起始治疗。在BOP注射后，第1组和第2组分别饲喂添加1000或500 ppm PCA的饲料49周。第3组动物仅用BOP处理。第4-6组中的动物，每组由10只仓鼠组成，给予1000或500 ppm PCA，或仅给予基础饮食而不预先注射BOP。在实验第52周结束时，BOP治疗组之间胰腺肿瘤病变的发生率和多重性相当。然而，PCA处理的高剂量组中大于3cm的胰腺肿瘤的发生率显著低于对照组（p < 0.05）。此外，PCA治疗降低了直接侵入邻近组织如横膈膜、脾和胃的晚期胰腺癌的发生率，第2组显著（p < 0.01）低于第3组。因此，我们的研究结果表明，PCA可以抑制BOP诱导的仓鼠胰腺癌发生的后期启动或进展阶段。
The chemopreventive effects of protocatechuic acid (PCA) were investigated during the post-initiation stage of the N-nitrosobis(2-oxopropyl)amine (BOP)-initiated hamster pancreatic tumorigenesis model. Female 5-week-old hamsters were divided into 6 groups. Animals in groups 1-3, each consisting of 30 hamsters, were given two s.c. injections of 20 mg/kg body weight of BOP with a one week interval as an initiation treatment. After the BOP injection, hamsters in groups 1 and 2 were respectively fed diet supplemented with 1000 or 500 ppm of PCA for 49 weeks. The animals in group 3 were treated with BOP alone. The animals in groups 4-6, each consisting of 10 hamsters, were given 1000 or 500 ppm PCA, or basal diet alone without prior BOP injection. At the termination of experimental week 52, the incidences and multiplicities of neoplastic lesions in the pancreas were comparable among the BOP-treated groups. However, the incidence of pancreatic tumors larger than 3 cm was significantly lower in the PCA-treated high dose groups than in the control group (p < 0.05). Moreover the incidence of advanced pancreatic cancers which had directly invaded adjacent tissues such as the diaphragm, spleen and stomach was reduced by the PCA treatments, being significantly (p < 0.01) lower in group 2 than in group 3. Our results thus indicated that PCA can inhibit the late post-initiation or progression phase of BOP-induced pancreatic carcinogenesis in hamsters.