NDLI: Nrf2-mediated liver protection by esculentoside A against acetaminophen toxicity through the AMPK/Akt/GSK3ß pathway.

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Nrf2-mediated liver protection by esculentoside A against acetaminophen toxicity through the AMPK/Akt/GSK3ß pathway.

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Nrf2-mediated liver protection by esculentoside A against acetaminophen toxicity through the AMPK/Akt/GSK3ß pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Lidong Zhang, Songling Cheng, Hang Lv, Hongming Cheng, Genhong Ci, Xinxin
Description	Country affiliation: China Author Affiliation: Wang L ( Institute of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, China.); Zhang S ( Department of Obstetrics and Gynecology, the First Hospital of Jilin University, Changchun 130021, China.); Cheng H ( Institute of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, China.); Lv H ( Institute of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, China.); Cheng G ( Institute of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, China); Ci X ( Institute of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, China. Electronic address: cixinxin@jlu.edu.cn.)
Abstract	Acetaminophen (APAP) overdose accounts for the majority of acute liver failure cases, and oxidative stress plays a key role in its toxic effects. Esculentoside A (EsA) has anti-oxidant activities, but its therapeutic potential for APAP hepatotoxicity remains unknown. This study aimed to assess the protective effects and mechanism of EsA against APAP-induced hepatotoxicity in vitro and in vivo. In vitro, EsA treatment inhibited APAP- or H O -induced cytotoxicity, H O and O production, glutathione (GSH) depletion and apoptosis dependent on nuclear factor erythroid-2-related factor 2 (Nrf2) activation in HepG2 cells. Moreover, EsA significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and serine/threonine kinase (Akt), as well as glycogen synthase kinase 3 beta (GSK-3ß) inhibitory phosphorylation at Ser9. Furthermore, an AMPK inhibitor (compound c) abolished the effects of EsA on AKT phosphorylation, GSK-3ß inactivation, Nrf2 nuclear translocation and cytoprotection. With regard to APAP-induced acute liver injury, EsA attenuated the APAP-stimulated increases in the serum ALT and AST levels, as well as centrilobular necrosis and GSH depletion in the mice. In addition, it decreased the GSSG level, GSSG-to-GSH ratio, and the phosphorylation and mitochondrial translocation of c-Jun N-terminal kinase (JNK). Further, the protective potential of EsA against mitochondrial dysfunction was exhibited not only by inhibiting Bax mitochondrial translocation and the release of mitochondrial inter-membrane proteins, such as apoptosis-inducing factor (AIF), but also by activating Nrf2/HO-1. Collectively, our findings suggest that EsA has protective potential against APAP toxicity by potentiating the Nrf2-regulated survival mechanism through the AMPK/Akt/GSK3ß pathway.
File Format	HTM / HTML
ISSN	08915849
Journal	Free Radical Biology and Medicine
Volume Number	101
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2016-12-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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