title: Lutein protects against β-amyloid peptide-induced oxidative stress in cerebrovascular endothelial cells through modulation of Nrf-2 and NF-κb.
abstract: In the present study, we determined the protective role of lutein against Aβ25-35peptide-induced oxidative stress and apoptosis in bEND.3 cells. Cell viability was determined through MTT assay. Reactive oxygen species, lipid peroxides, and antioxidant enzyme activities were evaluated to analyze the oxidative stress status. NF-κB and Nrf-2 downstream target protein expressions were determined through western blot. Apoptosis was analyzed through caspase activities and subG1 accumulation. The results showed that Aβ25-35significantly increased (p < 0.001) oxidative stress biomarkers. Aβ25-35significantly up-regulated NF-κB nuclear expression and down-regulated Nrf-2 levels and HO-1 and, NQO-1 expressions. Aβ25-35induced apoptosis through decreasing mitochondrial membrane potential and increasing caspase 9 and 3 activities. Lutein pre-treatment significantly (p < 0.001) improved cell viability and decreased ROS levels (p < 0.001) and lipid peroxidation (p < 0.01). Lutein prevented Aβ25-35-induced NF-κB nuclear expressions and up-regulated Nrf-2 expressions. Further, lutein also improved mitochondrial membrane potential and down-regulated caspase activities and subG1 accumulation. The present study shows the protective role of lutein against Aβ25-35-induced toxicity by modulating Nrf-2 and NF-κB expressions in cerebrovascular endothelial cells.
authors.affiliation: Department of Neurology, Tianjin Nankai Hospital, No.122, Sanwei Road, Nankai District, Tianjin, 300100, People's Republic of China. ltliutao06@hotmail.com.
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of Rehabilitation, Tianjin Fourth Central Hospital, Tianjin, 300140, China.
authors.forename: Wei-Hong
authors.initials: WH
authors.lastname: Liu
authors.affiliation: Department of Neurology, Tianjin Nankai Hospital, No.122, Sanwei Road, Nankai District, Tianjin, 300100, People's Republic of China.
authors.forename: Jin-Sheng
authors.initials: JS
authors.lastname: Zhao
authors.affiliation: Department of Neurology, Tianjin Nankai Hospital, No.122, Sanwei Road, Nankai District, Tianjin, 300100, People's Republic of China.
authors.forename: Fan-Zheng
authors.initials: FZ
authors.lastname: Meng
authors.affiliation: Department of Neurology, Tianjin Nankai Hospital, No.122, Sanwei Road, Nankai District, Tianjin, 300100, People's Republic of China.
authors.forename: Heng
authors.initials: H
authors.lastname: Wang
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006801:Humans; D014975:Lutein / Q000494:pharmacology*; D008954:Models, Biological; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D021381:Protein Transport / Q000187:drug effects; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D016229:Amyloid beta-Peptides; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; D018696:Neuroprotective Agents; D051547:Heme Oxygenase-1; D016660:NAD(P)H Dehydrogenase (Quinone); C447479:NQO1 protein, human; D014975:Lutein
keywords: Apoptosis; Aβ 25–35; Lutein; NF-κB; Nrf-2; Oxidative stress