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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 2752389, 12 pages
Research Article

The Ethanol Extract of Licorice (Glycyrrhiza uralensis) Protects against Triptolide-Induced Oxidative Stress through Activation of Nrf2

1Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha 410011, China
2Institute of Clinical Pharmacy, Central South University, Changsha 410011, China
3School of Pharmaceutical Sciences, Central South University, Changsha 410013, China
4School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410028, China
5Department of Pharmacy, Chemistry College, Xiangtan University, Xiangtan 411105, China

Correspondence should be addressed to Miao Yan; moc.621@uscoaimnay

Received 7 June 2017; Revised 29 July 2017; Accepted 14 August 2017; Published 26 September 2017

Academic Editor: Yoshiji Ohta

Copyright © 2017 Ling-Juan Cao 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.


To investigate the potential role of nuclear factor erythroid 2-related factor 2 (Nrf2) in licorice ethanol extract (LEE) against triptolide- (TP-) induced hepatotoxicity, HepG2 cells were exposed to LEE (30, 60, and 90 mg·L−1) for 12 h and then treated with TP (50 nM) for 24 h. Besides, an acute liver injury model was established in ICR mice by a single dose of TP (1.0 mg·kg−1, i.p.). Relevant oxidant and antioxidant mediators were analyzed. TP led to an obvious oxidative stress as evidenced by increasing levels of ROS and decreasing GSH contents in HepG2 cells. In vitro results were likely to hold true in in vivo experiments. LEE protected against TP-induced oxidative stress in both in vitro and in vivo conditions. Furthermore, the decreased level of Nrf2 in the TP-treated group was observed. The mRNA levels of downstream genes decreased as well in ICR mice liver, whereas they increased in HepG2 cells. In contrast, LEE pretreatment significantly increased the level of Nrf2 and its downstream genes. LEE protects against TP-induced oxidative stress partly via the activation of Nrf2 pathway.