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Hesperetin protects against H2O2-triggered oxidative damage via upregulation of the Keap1-Nrf2/HO-1 signal pathway in ARPE-19 cells.
Biomed Pharmacother. 2017 Apr; 88:124-133.BP

Abstract

Age-related macular degeneration (AMD) is an irreversible vision loss disease that primarily results from oxidative stress that causes oxidative damage to the retinal pigment epithelial (RPE) cells. Hesperetin (Hesp) is a common flavanone glycoside compound that has been demonstrated to exhibit a variety of biological and pharmacological properties that include anti-inflammatory and antioxidant properties. The aim of this study is to explore the ability of Hesp to attenuate oxidative damage in hydrogen peroxide (H2O2)-stimulated ARPE-19 cells. The results indicated that Hesp treatment not only increased cell survival but also decreased reactive oxygen species (ROS) generation, whereas these roles were effectively enhanced the superoxide dismutase (SOD) and glutathione (GSH) levels, and reduced malondialdehyde (MDA) formation. Importantly, the level of heme oxygenase-1 (HO-1) expression was increased by Hesp exposure, which resulted in a decrease after the transfection of cells with Nrf2-siRNA. Additionally, further results revealed that Hesp treatment significantly elevated Keap-1 protein expression, Nrf2 nuclear translocation and ARE activities. These observations indicated that Hesp treatment effectively protected against H2O2-induced oxidative damage in ARPE-19 cells by inhibiting cell apoptosis, ROS overproduction and MDA formation as well as enhancing the SOD and GSH levels. The underlying mechanisms may be related to the activation of the Keap1-Nrf2/HO-1 signal pathway, which may provide biological evidence to further encourage the investigation of the protective effect of Hesp in AMD disease.

Authors+Show Affiliations

Department of Ophthalmology, Second Hospital of Jilin University, Changchun 130041, China.Department of Ophthalmology, Second Hospital of Jilin University, Changchun 130041, China.Department of Ophthalmology, First Hospital of Jilin University, Changchun 130021, China, China.Department of Ophthalmology, First Hospital of Jilin University, Changchun 130021, China, China. Electronic address: lvhm63251@163.com.Department of Ophthalmology, First Hospital of Jilin University, Changchun 130021, China, China. Electronic address: cz3531@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28103505

Citation

Zhu, Chao, et al. "Hesperetin Protects Against H2O2-triggered Oxidative Damage Via Upregulation of the Keap1-Nrf2/HO-1 Signal Pathway in ARPE-19 Cells." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 88, 2017, pp. 124-133.
Zhu C, Dong Y, Liu H, et al. Hesperetin protects against H2O2-triggered oxidative damage via upregulation of the Keap1-Nrf2/HO-1 signal pathway in ARPE-19 cells. Biomed Pharmacother. 2017;88:124-133.
Zhu, C., Dong, Y., Liu, H., Ren, H., & Cui, Z. (2017). Hesperetin protects against H2O2-triggered oxidative damage via upregulation of the Keap1-Nrf2/HO-1 signal pathway in ARPE-19 cells. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 88, 124-133. https://doi.org/10.1016/j.biopha.2016.11.089
Zhu C, et al. Hesperetin Protects Against H2O2-triggered Oxidative Damage Via Upregulation of the Keap1-Nrf2/HO-1 Signal Pathway in ARPE-19 Cells. Biomed Pharmacother. 2017;88:124-133. PubMed PMID: 28103505.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hesperetin protects against H2O2-triggered oxidative damage via upregulation of the Keap1-Nrf2/HO-1 signal pathway in ARPE-19 cells. AU - Zhu,Chao, AU - Dong,Yuchen, AU - Liu,Haile, AU - Ren,Hua, AU - Cui,Zhihua, Y1 - 2017/01/16/ PY - 2016/09/18/received PY - 2016/11/15/revised PY - 2016/11/21/accepted PY - 2017/1/20/pubmed PY - 2017/3/28/medline PY - 2017/1/20/entrez KW - AMD KW - HO-1 KW - Hesperetin KW - Nrf2 KW - Oxidative stress SP - 124 EP - 133 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 88 N2 - Age-related macular degeneration (AMD) is an irreversible vision loss disease that primarily results from oxidative stress that causes oxidative damage to the retinal pigment epithelial (RPE) cells. Hesperetin (Hesp) is a common flavanone glycoside compound that has been demonstrated to exhibit a variety of biological and pharmacological properties that include anti-inflammatory and antioxidant properties. The aim of this study is to explore the ability of Hesp to attenuate oxidative damage in hydrogen peroxide (H2O2)-stimulated ARPE-19 cells. The results indicated that Hesp treatment not only increased cell survival but also decreased reactive oxygen species (ROS) generation, whereas these roles were effectively enhanced the superoxide dismutase (SOD) and glutathione (GSH) levels, and reduced malondialdehyde (MDA) formation. Importantly, the level of heme oxygenase-1 (HO-1) expression was increased by Hesp exposure, which resulted in a decrease after the transfection of cells with Nrf2-siRNA. Additionally, further results revealed that Hesp treatment significantly elevated Keap-1 protein expression, Nrf2 nuclear translocation and ARE activities. These observations indicated that Hesp treatment effectively protected against H2O2-induced oxidative damage in ARPE-19 cells by inhibiting cell apoptosis, ROS overproduction and MDA formation as well as enhancing the SOD and GSH levels. The underlying mechanisms may be related to the activation of the Keap1-Nrf2/HO-1 signal pathway, which may provide biological evidence to further encourage the investigation of the protective effect of Hesp in AMD disease. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/28103505/Hesperetin_protects_against_H2O2_triggered_oxidative_damage_via_upregulation_of_the_Keap1_Nrf2/HO_1_signal_pathway_in_ARPE_19_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(16)31648-1 DB - PRIME DP - Unbound Medicine ER -