The anti-inflammatory profile of DPA was investigated through LPS-induced RAW264.7 cells. Inflammatory mediators （NO， PGE2） and cytokines （TNF-α， IL-1β， IL-6 and IL-10） were used to assess the anti-inflammatory ability of DPA. Moreover， the molecular mechanisms underlying this effect were also explored from the perspective of NF-κB signal pathway. The results showed that DPA could significantly inhibit the excess production of NO and PGE2 by suppressing the protein expression of iNOS and COX-2. Besides， DPA also inhibited the abnormal production and mRNA expression of pro-inflammatory cytokines， namely TNF-α， IL-1β and IL-6 and promoted the production and mRNA expression of anti-inflammation cytokine， IL-10. Furthermore， the LPS-induced activation of NF-κB was significantly inhibited by DPA （stronger than EPA and DHA）. Thus， the entry of p50/p65 into nucleus to bind to the inflammatory gene site and the resulting inflammation were suppressed.