Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells
Joint Authors
Lv, Hongming
Ren, Hua
Wang, Lidong
Chen, Wei
Ci, Xinxin
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-10-20
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Licochalcone A (Lico A) exhibits various biological properties, including anti-inflammatory and antioxidant activities.
In this study, we investigated the antioxidative potential and mechanisms of Lico A against tert-butyl hydroperoxide- (t-BHP-) induced oxidative damage in RAW 264.7 cells.
Our results indicated that Lico A significantly inhibited t-BHP-induced cytotoxicity, apoptosis, and reactive oxygen species (ROS) generation and reduced glutathione (GSH) depletion but increased the glutamate-cysteine ligase modifier (GCLM) subunit and the glutamate-cysteine ligase catalytic (GCLC) subunit genes expression.
Additionally, Lico A dramatically upregulated the antioxidant enzyme heme oxygenase 1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2), which were associated with inducing Nrf2 nuclear translocation, decreasing Keap1 protein expression and increasing antioxidant response element (ARE) promoter activity.
Lico A also obviously induced the activation of serine/threonine kinase (Akt) and extracellular signal-regulated kinase (ERK), but PI3K/Akt and ERK inhibitors treatment displayed clearly decreased levels of LicoA-induced Nrf2 nuclear translocation and HO-1 expression, respectively.
Furthermore, Lico A treatment markedly attenuated t-BHP-induced oxidative damage, which was reduced by treatment with PI3K/Akt, ERK, and HO-1 inhibitors.
Therefore, Lico A might have a protective role against t-BHP-induced cytotoxicity by modulating HO-1 and by scavenging ROS via the activation of the PI3K/Akt and ERK/Nrf2 signaling pathways.
American Psychological Association (APA)
Lv, Hongming& Ren, Hua& Wang, Lidong& Chen, Wei& Ci, Xinxin. 2015. Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-13.
https://search.emarefa.net/detail/BIM-1075741
Modern Language Association (MLA)
Lv, Hongming…[et al.]. Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells. Oxidative Medicine and Cellular Longevity No. 2015 (2015), pp.1-13.
https://search.emarefa.net/detail/BIM-1075741
American Medical Association (AMA)
Lv, Hongming& Ren, Hua& Wang, Lidong& Chen, Wei& Ci, Xinxin. Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells. Oxidative Medicine and Cellular Longevity. 2015. Vol. 2015, no. 2015, pp.1-13.
https://search.emarefa.net/detail/BIM-1075741
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1075741