Table of Contents Author Guidelines Submit a Manuscript
Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 9253462, 15 pages
https://doi.org/10.1155/2017/9253462
Research Article

Activation of AMPK by Buddleja officinalis Maxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress

1MRC-GHF, College of Korean Medicine, Daegu Haany University, Gyeongsan 38610, Republic of Korea
2HaniBio Co., Ltd., Gyeongsan 712-260, Republic of Korea
3Division of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan 626-870, Republic of Korea
4School of Mental Health, Qiqihar Medical University, Qiqihar, Heilongjiang 161042, China

Correspondence should be addressed to Rongjie Zhao; moc.oohay@eijgnor_oahz and Sang Chan Kim; rk.ca.uhd@mikcs

Received 30 December 2016; Accepted 6 March 2017; Published 3 April 2017

Academic Editor: Roberto K. N. Cuman

Copyright © 2017 Ji Yun Jung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders.