Eicosapentaenoic acid prevents lipopolysaccharide-stimulated DNA binding of activator protein-1 and c-Jun N-terminal kinase activity

Eicosapentaenoic acid inhibits UV-induced MMP-1 expression in human dermal fibroblasts

“…The inhibition of AP-1 activity by EPA has also been reported in lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells (41) and TPA-stimulated mouse epidermal JB6 cells (42). Consistent with our results, EPA pretreatment was also found to attenuate increases of c-Jun and c-Fos protein levels by lipopolysaccharide and AP-1 DNA binding activity, which are all related to the inhibition of lipopolysaccharide-induced TNF-␣ expression by EPA (36). Moreover, phosphorylation of c-Jun by JNK is known to stimulate AP-1 transactivation activity (22, 43, 44).…”

“…Therefore, our data indicate that EPA may prevent UV-induced MMP-1 expression by inhibiting the UV-induced activation of ERK and JNK. Recent studies have shown that EPA modulates the ERK1/2 signaling induced by PMA via protein kinase C-dependent and -independent pathways in human T-cells (35) and also inhibits lipopolysaccharide-induced JNK activation (36). Although p38 MAPK induces c-Jun expression by enhancing ATF2 transcriptional activity, the inhibition of p38 kinase activity by pretreating HDFs with SB203580 was not found to change UV-induced MMP-1 expression in the present study.…”

Eicosapentaenoic Acid Prevents Saturated Fatty Acid-Induced Vascular Endothelial Dysfunction: Involvement of Long-Chain Acyl-CoA Synthetase

“…Because p21 expression was not attenuated by IKK inhibitor in our investigation, the PAinduced increase in p21 expression may be a factor independent of the IKK-NF-kB pathway. It has been demonstrated that in THP-1 macrophages, PA stimulates the phosphorylation of p38 MAPK while EPA inhibits it 11) , and EPA has also been shown to inhibit LPS-induced AP-1 activation 34) . Therefore, the changes in p21 expression in vascular endothelial cells induced by PA or EPA are consistent with previous reports.…”

n-3 Fatty acids block TNF-α-stimulated MCP-1 expression in rat mesangial cells

“…Based on studies in other cell systems, we hypothesized that an AP-1 binding site located within the proximal promoter region may be involved in n-3 fatty acid-mediated inhibition of TNF-␣-stimulated MCP-1 transcription (4,43,59,72,76,80). We found that a mutant MCP-1 construct with deletion of an AP-1 site located within the promoter region in addition to the distal B1 and B2 elements shows no transcriptional activation in response to TNF-␣, as expected, and no transcriptional suppression in response to DHA and EPA.…”