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粗大豆胰蛋白酶抑制剂对N-亚硝基双(2-氧代丙基)胺启动后仓鼠胰腺导管癌变的抑制作用。

Inhibitory effects of crude soybean trypsin inhibitor on pancreatic ductal carcinogenesis in hamsters after initiation with N-nitrosobis(2-oxopropyl)amine.

作者信息

Furukawa F, Nishikawa A, Imaida K, Mitsui M, Enami T, Hayashi Y, Takahashi M

机构信息

Division of Pathology, National Institute of Health Sciences, Tokyo, Japan.

出版信息

Carcinogenesis. 1992 Nov;13(11):2133-5. doi: 10.1093/carcin/13.11.2133.

Abstract

The effects of soybean trypsin inhibitor (SBTI) administration during the promotion phase of pancreatic carcinogenesis were investigated. Female Syrian golden hamsters were given three weekly s.c. injections of N-nitrosobis(2-oxopropyl)amine (BOP) each at a dose of 10 mg/kg and then administered 5% SBTI diet for the following 37 weeks. Additional groups of animals received the BOP injection alone or the 5% SBTI diet alone as controls. At week 40 of the experiment, all surviving animals were killed and development of pancreatic lesions was assessed histopathologically. The results showed that the incidence of dysplastic lesions in hamsters of the BOP/SBTI group was significantly decreased as compared to that of the BOP group (P < 0.01). A similar but not significant tendency was also found for pancreatic adenocarcinomas. In addition, the number of dysplastic lesions in the pancreas head portion in the BOP/SBTI group were significantly decreased as compared to the BOP group value (P < 0.05). Furthermore, atrophic changes of the pancreatic exocrine tissue were more severe in the BOP group than in the BOP/SBTI group (P < 0.01), indicating that SBTI treatment gave effective protection against the replacement process of acinar cell induced by BOP. Thus, the present experiment demonstrated that SBTI can inhibit hamster pancreatic ductal carcinogenesis when given in the promotion phase, in clear contrast to the enhancing effects reported for preneoplastic acinar lesion development in rats.

摘要

研究了在胰腺癌发生促进阶段给予大豆胰蛋白酶抑制剂(SBTI)的效果。雌性叙利亚金黄地鼠每周皮下注射3次N-亚硝基双(2-氧代丙基)胺(BOP),每次剂量为10mg/kg,然后在接下来的37周给予5% SBTI饮食。另外几组动物分别单独接受BOP注射或单独接受5% SBTI饮食作为对照。在实验第40周,处死所有存活动物,通过组织病理学评估胰腺病变的发展情况。结果显示,与BOP组相比,BOP/SBTI组仓鼠发育异常病变的发生率显著降低(P<0.01)。胰腺腺癌也有类似但不显著的趋势。此外,与BOP组相比,BOP/SBTI组胰头部分发育异常病变的数量显著减少(P<0.05)。此外,BOP组胰腺外分泌组织的萎缩变化比BOP/SBTI组更严重(P<0.01),表明SBTI治疗对BOP诱导的腺泡细胞替代过程提供了有效的保护。因此,本实验表明,在促进阶段给予SBTI可抑制仓鼠胰腺导管癌发生,这与报道的SBTI对大鼠肿瘤前腺泡病变发展的促进作用形成鲜明对比。

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