Inhibitory effect on α-glucosidase by Adhatoda vasica Nees

被引：79

作者：

Gao, Hong ^{[1
]}

Huang, Yi-Na ^{[2
]}

Gao, Bo ^{[2
]}

Li, Peng ^{[1
]}

Inagaki, Chika ^{[1
]}

Kawabata, Jun ^{[1
]}

机构：

[1] Hokkaido Univ, Grad Sch Agr, Div Appl Biosci, Kita Ku, Sapporo, Hokkaido 0608589, Japan

[2] Sichuan Univ, Dept Publ Hlth, Hua Xi Med Ctr, Chengdu 610064, Peoples R China

来源：

FOOD CHEMISTRY | 2008年 / 108卷 / 03期

基金：

日本学术振兴会;

关键词：

alpha-glucosidase; sucrase inhibitor; postprandial hyperglycemia; Adhatoda vasica;

D O I：

10.1016/j.foodchem.2007.12.002

中图分类号：

O69 [应用化学];

学科分类号：

081704 [应用化学];

摘要：

Methanolic extracts from the medicinal parts of 40 traditional Chinese herbs were tested in screening experiments for rat intestinal alpha-glucosidase. The methanolic extract from the leaves of Adhatoda vasica Nees (Acanthaceae) showed the highest sucrase inhibitory activity with sucrose as a substrate. Enzyme assay-guided fractionation of this extract afforded vasicine (1) and vasicinol (2), and the structures of these compounds were elucidated on the basis of MS and NMR analysis. Compounds 1 and 2 showed a high sucrase inhibitory activity, and the IC50 values were 125 mu M and 250 mu M, respectively. Both 1 and 2 were shown to be reversible inhibitors of sucrase. Kinetic data revealed that compounds 1 and 2 inhibited sucrose-hydrolysing activity of rat intestinal alpha-glucosidase competitively with K-i values of 82 mu M and 183 M, respectively. This is the first report on the mammalian alpha-glucosidase inhibition of A. vasica and the inhibitory effect on sucrase by 1 and 2 from this herb species. These results suggest a use of the extract of A. vasica as an antidiabetic agent and show a possibility that compounds 1 and 2 could be an useful treatment for metabolic disorders. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：965 / 972

页数：8

共 25 条

[1]

Brantner A. H., 1998, Pharmaceutical and Pharmacological Letters, V8, P137

[2]

Targeting postprandial hyperglycemia: A comparative study of insulinotropic agents in type 2 diabetes [J].