Journal
FRONTIERS IN IMMUNOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2019.00286
Keywords
Inonotus sanghuang; polyphenols; inflammation; obesity; NF-kappa B signaling; MAPK signaling
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Funding
- National Natural Science Foundation of China [81402677]
- Natural Science Foundation of Henan Province [182300410325]
- Projects of Henan Science and Technology Development [172102410036, 162300410116, 172102310151]
- Science Research program for Colleges and Universities of Hebei Province [ZD2018067]
- Key Project of Henan Education Committee [16A320037]
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Aims: Obesity is characterized as a chronic state of low-grade inflammation with progressive immune cell infiltration into adipose tissue. Adipose tissue macrophages play a critical role in the establishment of chronic inflammatory states and metabolic dysfunctions. Inonotus (I.) sanghuang and its extract polyphenols exhibit anti-carcinogenesis, anti-inflammatory, and anti-oxidant activities. However, the action of I. sanghuang polyphenols in obesity-related inflammation has not been reported. The aim of this study was to explore the anti-inflammatory action of polyphenols from I. sanghuang extract (ISE) in macrophages and the interaction between macrophages and adipocytes. Materials and Methods: RAW264.7 macrophages were stimulated with LPS or conditioned medium of hypertrophied 3T3-L1 adipocytes or cocultured with differentiated adipocytes in the presence of different doses of ISE. The inflammatory cytokines were evaluated by ELISA, the MAPK, NF-kappa B, and IL-6/STAT3 signals were determined by immunoblotting, and the migrated function of macrophages was determined by migration assay. Results: ISE suppressed the inflammatory mediators including NO, TNF-alpha, IL-6, and MCP-1 induced by either LPS or conditioned medium derived from 3T3-L1 adipocytes. ISE also decreased the production of these inflammatory mediators in cocultures of 3T3-L1 adipocytes and RAW264.7 macrophages. Furthermore, ISE blocked RAW264.7 macrophages migration toward 3T3-L1 adipocytes in cocultures. Finally, this effect of ISE might be mediated via inhibiting ERK, p38, and STAT3 activation. Conclusions: Our findings indicate the possibility that ISE suppresses the interaction between macrophages and adipocytes, attenuates chronic inflammation in adipose tissue and improves obesity-related insulin resistance and complication, suggesting that ISE might be a valuable medicinal food effective in improving insulin resistance and metabolic syndrome.
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