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Sargassum horneri (Turner) C. Agardh ethanol extract inhibits the fine dust inflammation response via activating Nrf2/HO-1 signaling in RAW 264.7 cells
BACKGROUND: Among the different kinds of pollution, air pollution continues to increase globally. East Asia is considered to be significantly affected. As a result, the populations in these regions face serious health issues including respiratory disorders. This study investigated the impact of fine...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131869/ https://www.ncbi.nlm.nih.gov/pubmed/30200963 http://dx.doi.org/10.1186/s12906-018-2314-6 |
Sumario: | BACKGROUND: Among the different kinds of pollution, air pollution continues to increase globally. East Asia is considered to be significantly affected. As a result, the populations in these regions face serious health issues including respiratory disorders. This study investigated the impact of fine dust (FD) particles (CRM No. 28) on macrophage cells as a model for alveolar lung cells. METHODS: The research focused on inflammation and oxidative stress induced by FD and Sargassum horneri (Turner) C. Agardh ethanol extract (SHE) as a potential treatment. S. horneri is a type of brown algae that has demonstrated anti-inflammatory effects against RAW 264.7 macrophages in previous studies. MTT, Griess, ELISA, western blotting, and mRNA expression analyses using PCR techniques were used in this study. RESULTS: The optimum FD concentration was determined to be 125 μg mL(− 1). FD particles stimulated inflammatory mediators production (iNOS, COX-2, and PGE(2)) and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), leading to NO production. These mediators were dose-dependently downregulated by treatment with SHE. IL-6 and TNF-α were identified as biomarkers for FD. SHE treatment induced HO-1 and Nrf2 activity in a dose-dependent manner under FD stimulation. This confirmed the cytoprotective effect against oxidative stress induced via FD. Furthermore, treatment of the cells with a p38 MAPK inhibitor (SB202190) induced FD-stimulated NO production. CONCLUSIONS: The results suggest that SHE increases macrophage cellular resistance to FD-induced inflammation and oxidative stress, probably via the p38 MAPK pathway and Nrf2/HO-1 expression. |
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