[Objective] The aim is to study the effects of ligustrazine on the lipopolysaccharide (LPS)-induced inflammation activated through arachidonicacid (AA) pathway, which would provide the experimental basis for extending the clinical application of ligustrazine. [Method] The effects of ligustrazine (1 and 10 μmol/L, 6 h) on the expression levels of COX-2, 5-LOX and FLAP were investigated in LPS-treated (1 mg/L, 2 h) primary human coronary artery endothelial cells. The expression level of above proteins as well as p-P38MAPK and p-STAT3 were also studied when SB203580 (20 μmol/L, 6 h), the inhibitor of p-P38MAPK, or AG490 (20 μmol/L, 6 h), the inhibitor of JAK2, was added at the same time with ligustrazine. [Result] Ligustrazine obviously inhibited the expression levels of 5-LOX and FLAP, as well as the phosphorylation activation of MAPK and STAT pathways. [Conclusion] Ligustrazine targeted on endothelial cells can inhibit inflammation activated through AA pathway, as well as the activation of MAPK and JAK2/STAT3 pathways. [Objective] The aim is to study the effects of ligustrazine on the lipopolysaccharide (LPS) -induced inflammation activated through arachidonic acid (AA) pathway, which would provide the experimental basis for extending the clinical application of ligustrazine. [Method] The effects of ligustrazine (1 and 10 μmol / L for 6 h) on the expression levels of COX-2, 5-LOX and FLAP were investigated in LPS-treated (1 mg / L, 2 h) primary human coronary artery endothelial cells of the above proteins as well as p-P38MAPK and p-STAT3 were also studied when SB203580 (20 μmol / L, 6 h), the inhibitor of p-P38 MAPK, or AG490 [Result] Ligustrazine obviously inhibited the expression levels of 5-LOX and FLAP, as well as the phosphorylation activation of MAPK and STAT pathways. [Conclusion] Ligustrazine targeted on endothelial cells can inhibit inflammation activated through AA pathway, as well as the activat ion of MAPK and JAK2 / STAT3 pathways.