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Astaxanthin protects ARPE-19 cells from oxidative stress via upregulation of Nrf2-regulated phase II enzymes through activation of PI3K/Akt.
Mol Vis. 2013; 19:1656-66.MV

Abstract

PURPOSE

Oxidative stress on retinal pigment epithelial (RPE) cells is thought to play a crucial role in the development and progression of age-related macular degeneration. Astaxanthin (AST) is a carotenoid that shows significant antioxidant properties. This study was designed to investigate the protective effect of AST on ARPE-19 cells against oxidative stress and the possible underlying mechanism.

METHODS

ARPE-19 cells exposed to different doses of H2O2 were incubated with various concentrations of AST and cell viability subsequently detected with the (4-[3-[4-iodophenyl]-2-4(4-nitrophenyl)-2H-5- tetrazolio-1,3-benzene disulfonate]; WST-1) assay. The apoptosis rate and intracellular levels of reactive oxygen species (ROS) were measured with flow cytometry. NAD(P)H quinine oxidoreductase 1 (NQO1), hemeoxygenase-1 (HO-1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) expression were examined with real-time PCR and western blotting. The nuclear localization of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein and the expression levels of cleaved caspase-3 and protein kinase B proteins were evaluated with western blotting.

RESULTS

AST clearly reduced H2O2-induced cell viability loss, cell apoptosis, and intracellular generation of ROS. Furthermore, treatment with AST activated the Nrf2-ARE pathway by inducing Nrf2 nuclear localization. Consequently, Phase II enzymes NQO1, HO-1, GCLM, and GCLC mRNA and proteins were increased. AST inhibited expression of H2O2-induced cleaved caspase-3 protein. Activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway was involved in the protective effect of AST on the ARPE-19 cells.

CONCLUSIONS

AST protected ARPE-19 cells against H2O2-induced oxidative stress via Nrf2-mediated upregulation of the expression of Phase II enzymes involving the PI3K/Akt pathway.

Authors+Show Affiliations

Department of Ophthalmology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, P.R. China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

23901249

Citation

Li, Zhongrui, et al. "Astaxanthin Protects ARPE-19 Cells From Oxidative Stress Via Upregulation of Nrf2-regulated Phase II Enzymes Through Activation of PI3K/Akt." Molecular Vision, vol. 19, 2013, pp. 1656-66.
Li Z, Dong X, Liu H, et al. Astaxanthin protects ARPE-19 cells from oxidative stress via upregulation of Nrf2-regulated phase II enzymes through activation of PI3K/Akt. Mol Vis. 2013;19:1656-66.
Li, Z., Dong, X., Liu, H., Chen, X., Shi, H., Fan, Y., Hou, D., & Zhang, X. (2013). Astaxanthin protects ARPE-19 cells from oxidative stress via upregulation of Nrf2-regulated phase II enzymes through activation of PI3K/Akt. Molecular Vision, 19, 1656-66.
Li Z, et al. Astaxanthin Protects ARPE-19 Cells From Oxidative Stress Via Upregulation of Nrf2-regulated Phase II Enzymes Through Activation of PI3K/Akt. Mol Vis. 2013;19:1656-66. PubMed PMID: 23901249.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Astaxanthin protects ARPE-19 cells from oxidative stress via upregulation of Nrf2-regulated phase II enzymes through activation of PI3K/Akt. AU - Li,Zhongrui, AU - Dong,Xin, AU - Liu,Hongling, AU - Chen,Xi, AU - Shi,Huanqi, AU - Fan,Yan, AU - Hou,Dingshan, AU - Zhang,Xiaomei, Y1 - 2013/07/25/ PY - 2012/11/01/received PY - 2013/07/22/accepted PY - 2013/8/1/entrez PY - 2013/8/1/pubmed PY - 2013/9/26/medline SP - 1656 EP - 66 JF - Molecular vision JO - Mol. Vis. VL - 19 N2 - PURPOSE: Oxidative stress on retinal pigment epithelial (RPE) cells is thought to play a crucial role in the development and progression of age-related macular degeneration. Astaxanthin (AST) is a carotenoid that shows significant antioxidant properties. This study was designed to investigate the protective effect of AST on ARPE-19 cells against oxidative stress and the possible underlying mechanism. METHODS: ARPE-19 cells exposed to different doses of H2O2 were incubated with various concentrations of AST and cell viability subsequently detected with the (4-[3-[4-iodophenyl]-2-4(4-nitrophenyl)-2H-5- tetrazolio-1,3-benzene disulfonate]; WST-1) assay. The apoptosis rate and intracellular levels of reactive oxygen species (ROS) were measured with flow cytometry. NAD(P)H quinine oxidoreductase 1 (NQO1), hemeoxygenase-1 (HO-1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) expression were examined with real-time PCR and western blotting. The nuclear localization of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein and the expression levels of cleaved caspase-3 and protein kinase B proteins were evaluated with western blotting. RESULTS: AST clearly reduced H2O2-induced cell viability loss, cell apoptosis, and intracellular generation of ROS. Furthermore, treatment with AST activated the Nrf2-ARE pathway by inducing Nrf2 nuclear localization. Consequently, Phase II enzymes NQO1, HO-1, GCLM, and GCLC mRNA and proteins were increased. AST inhibited expression of H2O2-induced cleaved caspase-3 protein. Activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway was involved in the protective effect of AST on the ARPE-19 cells. CONCLUSIONS: AST protected ARPE-19 cells against H2O2-induced oxidative stress via Nrf2-mediated upregulation of the expression of Phase II enzymes involving the PI3K/Akt pathway. SN - 1090-0535 UR - https://www.unboundmedicine.com/medline/citation/23901249/Astaxanthin_protects_ARPE_19_cells_from_oxidative_stress_via_upregulation_of_Nrf2_regulated_phase_II_enzymes_through_activation_of_PI3K/Akt_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23901249/ DB - PRIME DP - Unbound Medicine ER -