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Hydrolyzed oyster extracts suppress lipopolysaccharide-mediated inflammation and oxidative stress in RAW264.7 murine macrophages
Oysters are rich nutrition sources that contain polysaccharides, proteins, peptides, phenolic compounds, minerals, and vitamins. In the search for compounds that exert anti-inflammatory effects in macrophages, we prepared hydrolyzed oyster ( Magallana gigas ) extracts (HOE) and evaluated their prote...
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Published in: | Biotechnology and bioprocess engineering 2024, 29(3), , pp.494-504 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Oysters are rich nutrition sources that contain polysaccharides, proteins, peptides, phenolic compounds, minerals, and vitamins. In the search for compounds that exert anti-inflammatory effects in macrophages, we prepared hydrolyzed oyster (
Magallana gigas
) extracts (HOE) and evaluated their protective effects against inflammation and oxidative stress in RAW264.7 murine macrophages treated with lipopolysaccharide (LPS). As expected, LPS notably stimulated the generation of inflammatory molecules and associated regulatory proteins. However, HOE effectively blocked these effects in a concentration-dependent manner. This suppressive effect of HOE on inflammation appears to be responsible for blocking nuclear factor-κB (NF-κB) signaling. In addition, LPS-mediated reactive oxygen species generation RAW264.7 cells was highly inhibited by HOE treatment, which appears to be partially regulated by nuclear factor erythroid 2-related factor 2 (Nrf2). Moreover, HOE at high concentrations inhibited pro-inflammatory mediators and cytokines to a greater extent than BAY7085, a pharmacological NF-κB inhibitor, in LPS-treated RAW264.7 cells. Taken together, our results show that HOE effectively inhibits inflammation and oxidative stress via modulating the NF-κB and/or Nrf2 signaling in RAW264.7 macrophages and can be a potential therapeutic agent to prevent inflammation-related diseases. |
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ISSN: | 1226-8372 1976-3816 |
DOI: | 10.1007/s12257-024-00094-6 |