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The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation

Triptolide (TP), an active ingredient of Tripterygium wilfordii Hook f., possesses a wide range of biological activities. Oxidative stress likely plays a role in TP-induced hepatotoxicity. Isoliquiritigenin (ISL) and glycyrrhetinic acid (GA) are potent hepatoprotection agents. The aim of the present...

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Autores principales: Cao, Ling-Juan, Li, Huan-De, Yan, Miao, Li, Zhi-Hua, Gong, Hui, Jiang, Pei, Deng, Yang, Fang, Ping-Fei, Zhang, Bi-Kui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745288/
https://www.ncbi.nlm.nih.gov/pubmed/26904149
http://dx.doi.org/10.1155/2016/8912184
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author Cao, Ling-Juan
Li, Huan-De
Yan, Miao
Li, Zhi-Hua
Gong, Hui
Jiang, Pei
Deng, Yang
Fang, Ping-Fei
Zhang, Bi-Kui
author_facet Cao, Ling-Juan
Li, Huan-De
Yan, Miao
Li, Zhi-Hua
Gong, Hui
Jiang, Pei
Deng, Yang
Fang, Ping-Fei
Zhang, Bi-Kui
author_sort Cao, Ling-Juan
collection PubMed
description Triptolide (TP), an active ingredient of Tripterygium wilfordii Hook f., possesses a wide range of biological activities. Oxidative stress likely plays a role in TP-induced hepatotoxicity. Isoliquiritigenin (ISL) and glycyrrhetinic acid (GA) are potent hepatoprotection agents. The aim of the present study was to investigate whether Nrf2 pathway is associated with the protective effects of ISL and GA against TP-induced oxidative stress or not. HepG2 cells were treated with TP (50 nM) for 24 h after pretreatment with ISL and GA (5, 10, and 20 μM) for 12 h and 24 h, respectively. The results demonstrated that TP treatment significantly increased ROS levels and decreased GSH levels. Both ISL and GA pretreatment decreased ROS and meanwhile enhanced intracellular GSH content. Additionally, TP treatment obviously decreased the protein expression of Nrf2 and its target genes including HO-1 and MRP2 except NQO1. Moreover, both ISL and GA displayed activities as inducers of Nrf2 and increased the expression of HO-1, NQO1, and MRP2. Taken together the current data confirmed that ISL and GA could activate the Nrf2 antioxidant response in HepG2 cells, increasing the expression of its target genes which may be partly associated with their protective effects in TP-induced oxidative stress.
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spelling pubmed-47452882016-02-22 The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation Cao, Ling-Juan Li, Huan-De Yan, Miao Li, Zhi-Hua Gong, Hui Jiang, Pei Deng, Yang Fang, Ping-Fei Zhang, Bi-Kui Evid Based Complement Alternat Med Research Article Triptolide (TP), an active ingredient of Tripterygium wilfordii Hook f., possesses a wide range of biological activities. Oxidative stress likely plays a role in TP-induced hepatotoxicity. Isoliquiritigenin (ISL) and glycyrrhetinic acid (GA) are potent hepatoprotection agents. The aim of the present study was to investigate whether Nrf2 pathway is associated with the protective effects of ISL and GA against TP-induced oxidative stress or not. HepG2 cells were treated with TP (50 nM) for 24 h after pretreatment with ISL and GA (5, 10, and 20 μM) for 12 h and 24 h, respectively. The results demonstrated that TP treatment significantly increased ROS levels and decreased GSH levels. Both ISL and GA pretreatment decreased ROS and meanwhile enhanced intracellular GSH content. Additionally, TP treatment obviously decreased the protein expression of Nrf2 and its target genes including HO-1 and MRP2 except NQO1. Moreover, both ISL and GA displayed activities as inducers of Nrf2 and increased the expression of HO-1, NQO1, and MRP2. Taken together the current data confirmed that ISL and GA could activate the Nrf2 antioxidant response in HepG2 cells, increasing the expression of its target genes which may be partly associated with their protective effects in TP-induced oxidative stress. Hindawi Publishing Corporation 2016 2016-01-21 /pmc/articles/PMC4745288/ /pubmed/26904149 http://dx.doi.org/10.1155/2016/8912184 Text en Copyright © 2016 Ling-Juan Cao et al. https://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Research Article
Cao, Ling-Juan
Li, Huan-De
Yan, Miao
Li, Zhi-Hua
Gong, Hui
Jiang, Pei
Deng, Yang
Fang, Ping-Fei
Zhang, Bi-Kui
The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title_full The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title_fullStr The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title_full_unstemmed The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title_short The Protective Effects of Isoliquiritigenin and Glycyrrhetinic Acid against Triptolide-Induced Oxidative Stress in HepG2 Cells Involve Nrf2 Activation
title_sort protective effects of isoliquiritigenin and glycyrrhetinic acid against triptolide-induced oxidative stress in hepg2 cells involve nrf2 activation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745288/
https://www.ncbi.nlm.nih.gov/pubmed/26904149
http://dx.doi.org/10.1155/2016/8912184
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