DPA体外抗炎活性及机制研究

Studies on the Anti-inflammatory Profile of DPA in Vitro and Its Mechanism

以脂多糖(LPS)诱导的RAW264.7巨噬细胞为炎症的体外模型,以炎症介质【NO和前列腺素E2(PGE2)】和炎症因子(TNF-α,IL-1β,IL-6和IL-10)为指标,研究二十二碳五烯酸(DPA)的体外抗炎活性,并从NF-κB代谢通路的角度探究DPA体外抗炎活性的作用机制。结果表明,DPA可以显著抑制iNOS和COX-2的表达,抑制炎症介质NO和PGE2的分泌,并且,DPA通过调控促炎因子(TNF-α,IL-1β,IL-6)和抑炎因子(IL-10)的平衡发挥抗炎作用。Western blot结果表明,DPA显著抑制NF-κB代谢通路中p50和p65的磷酸化,限制p50/p65核内转移,抑制炎症级联反应,发挥抗炎作用。

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-1βand 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.