Next Article in Journal
The Role of Gut Microbiota and Diet on Uremic Retention Solutes Production in the Context of Chronic Kidney Disease
Next Article in Special Issue
Molecular Mechanisms of Apoptosis in HepaRG Cell Line Induced by Polyphyllin VI via the Fas Death Pathway and Mitochondrial-Dependent Pathway
Previous Article in Journal
Crystal Structure of Botulinum Neurotoxin A2 in Complex with the Human Protein Receptor SV2C Reveals Plasticity in Receptor Binding
Article Menu
Issue 4 (April) cover image

Export Article

Open AccessArticle
Toxins 2018, 10(4), 154; https://doi.org/10.3390/toxins10040154

Bavachinin Induces Oxidative Damage in HepaRG Cells through p38/JNK MAPK Pathways

1,‡
,
2,‡
,
1, 1
,
1, 1,†,* and 1,†,*
1
Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100193, China
2
Harbin University of Commerce, Harbin 150076, China
Current Address: Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 151, Malianwa North Road, Haidian District, Beijing 100193, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 14 March 2018 / Revised: 8 April 2018 / Accepted: 10 April 2018 / Published: 12 April 2018
(This article belongs to the Special Issue Toxicity of Plant Toxins in Medical Herbs)
View Full-Text   |   Download PDF [17894 KB, uploaded 3 May 2018]   |  

Abstract

Drug-induced liver injury is one of the main causes of drug non-approval and drug withdrawal by the Food and Drug Administration (FDA). Bavachinin (BVC) is a natural product derived from the fruit of the traditional Chinese herb Fructus Psoraleae (FP). There have been reports of acute liver injury following the administration of FP and its related proprietary medicines. To explore BVC hepatotoxicity and its mechanisms, we used the HepaRG cell line. In our recent research, we showed that BVC induces HepaRG cell death, mainly via BVC-induced oxidative damage. The formation of ROS is closely related to the activation of the stress-activated kinases, JNK and p38, while SP600125 (SP, JNK inhibitor) and SB203580 (SB, p38 inhibitor) pretreatment inhibited the generation of ROS. On the other hand, N-acetylcysteine (NAC) pretreatment prevented the phosphorylation of p38 but not that of JNK. Taken together, these data reveal that BVC induces HepaRG cell death via ROS and the JNK/p38 signaling pathways. View Full-Text
Keywords: drug-induced liver injury; Bavachinin; reactive oxygen species; p38 MAPK; JNK MAPK drug-induced liver injury; Bavachinin; reactive oxygen species; p38 MAPK; JNK MAPK
Figures

Figure 1

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. (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Wang, S.; Wang, M.; Wang, M.; Tian, Y.; Sun, X.; Sun, G.; Sun, X. Bavachinin Induces Oxidative Damage in HepaRG Cells through p38/JNK MAPK Pathways. Toxins 2018, 10, 154.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Toxins EISSN 2072-6651 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top