n-Butyl-alpha-D-fructofuranoside Isolated from Ulmus davidiana Enhances Nrf2 Activity Through Activation of JNK
- Authors
- Choi, HJ[Choi, Hee-Jin]; Choi, HJ[Choi, Hee-Jung]; Park, MJ[Park, Mi-Joo]; Chung, TW[Chung, Tae-Wook]; Joo, M[Joo, Myungsoo]; Kim, CH[Kim, Cheorl-Ho]; Chang, HW[Chang, Hyun-Wook]; Son, JK[Son, Jong-Keun]; Ha, KT[Ha, Ki-Tae]
- Issue Date
- 2016
- Publisher
- BENTHAM SCIENCE PUBL LTD
- Keywords
- n-Butyl alpha-D-fructofuranoside; Ulmus davidiana; Nrf2; JNK; Macrophage; HO-1; NQO-1; Anti-inflammation
- Citation
- CURRENT PHARMACEUTICAL BIOTECHNOLOGY, v.17, no.13, pp.1181 - 1188
- Indexed
- SCIE
SCOPUS
- Journal Title
- CURRENT PHARMACEUTICAL BIOTECHNOLOGY
- Volume
- 17
- Number
- 13
- Start Page
- 1181
- End Page
- 1188
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/40615
- DOI
- 10.2174/1389201017666160920161238
- ISSN
- 1389-2010
- Abstract
- Background: The root bark of Ulmus davidiana Nakai (Ulmaceae), a traditional Korean medicinal plant, is used for treating inflammatory diseases. Objective: We investigated the Nrf2-activating effect of U. davidiana and identified a novel Nrf2 activator from its constituent compounds. Methods: Cytotoxicity was measured by MTT assay, and the Nrf2 activity was examined by luciferase-reporter assay and western blot analysis. The expression of Nrf2-dependent antioxidant genes was estimated by RT-PCR. The signal pathway related to Nrf2 activation was analyzed by treating specific signaling inhibitors. Anti-inflammatory effects were determined using an NO assay and western blot analysis. Results: Ulmus davidiana and its constituent compounds, including catechin-3-O-alpha-L-rhamnopyranoside, alpha-nigerose, n-butyl alpha-D-fructofuranoside (NBF), and procyanidin B3, enhanced the transcriptional activity of Nrf2. Of these compounds, only NBF possessed a distinctive structure and exhibited ROS-independent Nrf2 activation. In addition, NBF significantly increased the nuclear translocation of Nrf2 and the expression of Nrf2-dependent detoxifying enzymes, including HO-1 and NQO-1, in dose-dependent manner. The Nrf2 activation induced by NBF was mediated by the phosphorylation of JNK. Consequently, pretreatment with NBF inhibited the LPS-induced expression of pro-inflammatory genes. Conclusion: To the best of our knowledge, this is the first study to report on the Nrf2-activating effect of U. davidiana and NBF. Given the importance of Nrf2 as a negative regulator in various inflammatory diseases, NBF could be considered as a novel candidate for the prevention and treatment of inflammatory diseases.
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Collections - Science > Department of Biological Science > 1. Journal Articles
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