PMC:7335494 / 58200-59293 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"There are several pharmacological studies suggesting molecular targets for the anti-inflammatory effects of n-3 PUFAs and their metabolites: PPAR-γ, GPR120, CMKLR1 (known as ChemR23), BLT1(leukotriene B4 receptor 1), GPR32 and ALX/FPR2 (Im, 2012). Thus, resolvins E1 and D1 exhibited a higher affinity for these receptors compared to EPA or DHA. Chem R23 and BLT1 are receptors of resolvin E1, while GPR32 and ALX/FPR2, bind to lipoxin A4 and resolvin D1 with high affinity. GPR120 was reported to be a receptor of EPA and DHA (EC50 ~ 1–10 μM), while ALX/FPR2 to annexin I and lipoxin A4 (Serhan and Petasis, 2011). Furthermore, some studies on GPR120 KO mice suggest that n-3 PUFAs that activate GPR120, interact with β-arrestin 2, and suppress NF-κB activation and macrophage-mediated inflammatory responses (Oh et al., 2010). However, it is important to highlight that the in vivo anti-inflammatory effects of n-3 PUFAs in humans are minor and might only occur at high n-3 PUFA levels, it was demonstrated in vitro that BSA-conjugated n-3 PUFA are incapable of activating GPR120 (Im, 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