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Lycium barbarum polysaccharide protects HSF cells against ultraviolet-induced damage through the activation of Nrf2

BACKGROUND: Lycium barbarum polysaccharide (LBP) is considered an antioxidant agent. NF-E2-related factor-2 (Nrf2) is an important regulator for protection against UV damage. In this study, we verified the performance of LBP and the correlation between LBP and Nrf2. METHODS: HSF cells were treated w...

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Detalles Bibliográficos
Autores principales: Liang, Bihua, Peng, Liqian, Li, Runxiang, Li, Huaping, Mo, Ziyin, Dai, Xinyue, Jiang, Na, Liu, Qing, Zhang, Erting, Deng, Huiyan, Li, Zhenjie, Zhu, Huilan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5930781/
https://www.ncbi.nlm.nih.gov/pubmed/29743894
http://dx.doi.org/10.1186/s11658-018-0084-2
Descripción
Sumario:BACKGROUND: Lycium barbarum polysaccharide (LBP) is considered an antioxidant agent. NF-E2-related factor-2 (Nrf2) is an important regulator for protection against UV damage. In this study, we verified the performance of LBP and the correlation between LBP and Nrf2. METHODS: HSF cells were treated with LBP to determine dose and time dependencies. An antioxidant response element (ARE) reporter was designed to monitor the activity of the Nrf2 antioxidant pathway. RESULTS: For HSF cells, the optimal LBP treatment was 300 μg/ml for 3 h. The ARE-reporter assay showed that LBP could increase the robustness of p-Nrf2. Treatments with genistein and LY294002 reduced of nuclear p-Nrf2 after 24 h. LBP increased the level of nuclear Nrf2, which functions by both phosphorylation and nuclear translocation. Silencing Nrf2 led to increased reactive oxygen species (ROS) levels, lower cell viability, and decreased superoxide dismutase (SOD) and glutathione peroxidase (GSP-PX) levels. This induced a higher level of lipid peroxide (LPO). However, LBP could decrease the levels of ROS and LPO and enhance the levels of SOD and GSP-PX. CONCLUSION: LBP protects HSF cells against UV damage via the regulation of Nrf2.