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菜豆中肠激酶抑制剂导致大鼠小肠黏膜增生

Small intestinal mucosal hyperplasia caused by an enterokinase inhibitor from red kidney bean in rats.

作者信息

Tajiri H, Lee P C, Lebenthal E

出版信息

J Nutr. 1986 May;116(5):873-80. doi: 10.1093/jn/116.5.873.

Abstract

A specific enterokinase inhibitor (EKI) was purified from red kidney bean (RKB). Male weanling rats fed a diet containing this purified EKI (0.06%) for 6 d showed increases in mucosal weights, protein, DNA and lactic dehydrogenase contents in their small intestines compared to age-matched control rats fed a standard diet. Total mucosal EK and disaccharidase activities were, however, decreased in EKI-fed rats. Thus, oral consumption of EKI from RKB led to small intestinal mucosal hyperplasia in rats. The mucosal hyperplasia observed in EKI-fed rats is not likely due to decreased turnover of mucosal proteins as a result of reduced luminal proteases since luminal contents of trypsin, chymotrypsin and elastase in EKI-fed rats were similar to those of control rats. Enterokinase inhibitor may have a direct hyperplastic effect on the small intestine of rats.

摘要

从红芸豆(RKB)中纯化出一种特异性肠激酶抑制剂(EKI)。与喂食标准饮食的同龄对照大鼠相比,雄性断奶大鼠喂食含这种纯化EKI(0.06%)的饮食6天后,其小肠黏膜重量、蛋白质、DNA和乳酸脱氢酶含量增加。然而,喂食EKI的大鼠黏膜总肠激酶和双糖酶活性降低。因此,口服来自RKB的EKI会导致大鼠小肠黏膜增生。在喂食EKI的大鼠中观察到的黏膜增生不太可能是由于腔内蛋白酶减少导致黏膜蛋白周转降低所致,因为喂食EKI的大鼠腔内胰蛋白酶、糜蛋白酶和弹性蛋白酶的含量与对照大鼠相似。肠激酶抑制剂可能对大鼠小肠有直接的增生作用。

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