Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1

BAO Hua-yan; YAN Jun; LI Ke; LIU Peng

doi:10.3969/j.issn.1006-0111.2012.03.008

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Objective To examine effect of lipoxin A4 (LXA4), protectin D1 (ProD1) or resolvin D1 (RvD1) on the activity of NFκB and their action mechanism. Methods The CHO cells, stably expressing NFκB luciferase reporter gene, were treated with LPS, HSP70, HMGB1 or S100A4, in the presence or absence of 100 nmol/L of LXA4, ProD1 or RvD1 for 30 minutes. The activity of NFκB was detected with the luciferase assay. The content of tumor necrosis factor α (TNFα) in supernatant was measured by enzyme-1inked immunosorbent assay (ELISA) and the expression of NFκB in the nucleus was detected by immune blotting. Results The activity of NFκB and the level of TNFα in supernatant were significantly upregulated after treatment of the cells with LPS, HSP70, HMGB1 or S100A4, respectively. However, the NFκB activity and concentration of TNFα were lowered in the cells preincubated with LXA4, ProD1 or RvD1 as compared to the stimulated cells. Moreover, the lipids significantly decreased the content of NFκB in the nucleus. Conclusion LXA4, ProD1 or RvD1 could significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. LXA4, ProD1 and RvD1 showed the potential in the development of new anti-inflammatory therapeutics, which was required further research.

Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China

Received Date: 2012-03-23

Rev Recd Date: 2012-05-07

Key words:

lipoxin /
protectin /
resolvin /
NFκB /
inflammation

Abstract: Objective To examine effect of lipoxin A4 (LXA4), protectin D1 (ProD1) or resolvin D1 (RvD1) on the activity of NFκB and their action mechanism. Methods The CHO cells, stably expressing NFκB luciferase reporter gene, were treated with LPS, HSP70, HMGB1 or S100A4, in the presence or absence of 100 nmol/L of LXA4, ProD1 or RvD1 for 30 minutes. The activity of NFκB was detected with the luciferase assay. The content of tumor necrosis factor α (TNFα) in supernatant was measured by enzyme-1inked immunosorbent assay (ELISA) and the expression of NFκB in the nucleus was detected by immune blotting. Results The activity of NFκB and the level of TNFα in supernatant were significantly upregulated after treatment of the cells with LPS, HSP70, HMGB1 or S100A4, respectively. However, the NFκB activity and concentration of TNFα were lowered in the cells preincubated with LXA4, ProD1 or RvD1 as compared to the stimulated cells. Moreover, the lipids significantly decreased the content of NFκB in the nucleus. Conclusion LXA4, ProD1 or RvD1 could significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. LXA4, ProD1 and RvD1 showed the potential in the development of new anti-inflammatory therapeutics, which was required further research.

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Reference (16)

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Stimulation of NFκB activity by the agonist inhibition from Lipoxin A4, Protectin D1 and Resolvin D1

doi: 10.3969/j.issn.1006-0111.2012.03.008

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