OBJECTIVE： To study anti-inflammatory effect and mechanism of the luteolin·4， 4′ -dipyridy co-crystal. METHODS： Using macrophage RAW264.7 of normal mice as control， the inflammation model was established with lipopolysaccharide （LPS）-induced RAW264.7 cells. MTT assay was used to detect cells activity 2 h after treatment of different concentrations of luteolin （10， 20， 40， 80 μmol/L）， 4， 4′ -dipyridy （10， 20， 40， 80 μmol/L） and luteolin·4， 4′ -dipyridy co-crystal （10， 20， 40， 80 μmol/L）. The mRNA expression of iNOS and COX-2 in RAW264.7 cells at 40 μmol/L were determined by qRT-PCR. The protein expression of TNF-α and IL-6 in RAW264.7 cells at 40 μmol/L were determined by ELISA. The protein expression of NF-κB p65 in RAW264.7 cells at 40 μmol/L were determined by Western bolt. RESULTS： Compared with normal cells， the activity of RAW264.7 cells was decreased significantly after induced by LPS （P＜0.01）； mRNA expression of iNOS and COX-2， protein expression of TNF-α， IL-6 and NF-κB p65 were increased significantly （P＜0.01）. Both luteolin and luteolin·    4， 4′ -dipyridy co-crystal could enhance the activity of RAW264.7 cells after induced by LPS （P＜0.05 or P＜0.01） in concentration-dependent manner. 4， 4′ -dipyridy had no significant effect on the activity of RAW264.7 cells after induced by LPS. After luteolin and luteolin·4， 4′ -dipyridy co-crystal at 40 μmol/L， mRNA expression of iNOS and COX-2， protein expression of TNF-α， IL-6 and NF-κB p65 in RAW264.7 cells after induced by LPS were decreased significantly （P＜0.05 or P＜0.01）； the luteolin·4， 4′ -dipyridy co-crystal was better than luteolin （P＜0.05 or P＜0.01）. CONCLUSIONS： The luteolin·4， 4′ -dipyridy co-crystal can inhibit the generation of inflammatory factors by down-regulating NF-κB signal， and its anti-i nflammatory effect is better than luteolin.