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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.
Oxid Med Cell Longev. 2015; 2015:709845.OM

Abstract

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.

Authors+Show Affiliations

Institute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China ; Key Laboratory of Zoonosis Research, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun 130062, China.Institute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.Institute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.Key Laboratory of Zoonosis Research, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun 130062, China.Institute of Translational Medicine, Department of Ophthalmology, The First Hospital, Jilin University, Changchun 130001, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26576227

Citation

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, vol. 2015, 2015, p. 709845.
Lv H, Ren H, Wang L, 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. Oxid Med Cell Longev. 2015;2015:709845.
Lv, H., Ren, H., Wang, L., Chen, W., & Ci, X. (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, 2015, 709845. https://doi.org/10.1155/2015/709845
Lv H, 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. Oxid Med Cell Longev. 2015;2015:709845. PubMed PMID: 26576227.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Lv,Hongming, AU - Ren,Hua, AU - Wang,Lidong, AU - Chen,Wei, AU - Ci,Xinxin, Y1 - 2015/10/20/ PY - 2014/12/22/received PY - 2015/01/28/revised PY - 2015/02/07/accepted PY - 2015/11/18/entrez PY - 2015/11/18/pubmed PY - 2016/7/28/medline SP - 709845 EP - 709845 JF - Oxidative medicine and cellular longevity JO - Oxid Med Cell Longev VL - 2015 N2 - 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. SN - 1942-0994 UR - https://www.unboundmedicine.com/medline/citation/26576227/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_ L2 - https://dx.doi.org/10.1155/2015/709845 DB - PRIME DP - Unbound Medicine ER -