Fig 1: Suppression of NF-κB activation and CCL2 expression by EPA treatment in vitro. a Suppression of LPS-induced NF-κB activation by the pre-treatment with EPA. RAW264.7 cells were treated with EPA (300 μM) for 60 min and then stimulated with LPS (3.3 μg/ml) for additional 10 min. NF-κB activation was then assessed by Western blot analysis using the whole cell lysate. The representative images of Western blot analyses from two independent experiments for phosphorylated form of NF-κB p65 subunit (Ser536), NF-κB p65 subunit or α-tubulin served as an internal control are shown. b Suppression of LPS-induced Ccl2 expression by the pre-treatment with EPA. RAW264.7 cells were treated with EPA (300 μM, n = 6) or an agonist for GPR120, TUG-891 (3 μM, n = 7), for 60 min and then stimulated with LPS (3.3 μg/ml) for additional 60 min. Ccl2 expression was then assess by RT-PCR analyses. Data represents mean ± SD. Statistical analysis was done by a Kruskal-Wallis test. *p < 0.05. c Suppression of CCL2 expression in IA lesions by EPA in rats. EPA (1000 mg/kg/day) was administered in a rat model subjected to aneurysm induction once a day for 12 days and expression of CCL2 in IA lesions was then assessed by immunohistochemistry. The representative images from immunohistochemistry for CCL2 (green), nuclear staining by DAPI (blue), and merged images are shown. The image from immunostaining without a primary antibody for CCL2 is also shown as a negative control study in the lowest panel. Bar; 20 μm