PMC:7335494 / 59294-60243
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 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