期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 281, 期 47, 页码 35686-35698出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M603357200
关键词
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资金
- NHLBI NIH HHS [R01 HL058115-09, HL58115, R37 HL058115, HL075397, R01 HL075397, R01 HL068878, HL70146, HL64937, R01 HL064937-05A1, R01 HL070146, R01 HL064937, R01 HL058115, T32HL07457, HL068878] Funding Source: Medline
- NIGMS NIH HHS [S06GM08248, S06 GM008248] Funding Source: Medline
Nitroalkene derivatives of linoleic acid (LNO2) and oleic acid (OA-NO2) are present; however, their biological functions remain to be fully defined. Herein, we report that LNO2 and OA-NO2 inhibit lipopolysaccharide-induced secretion of proinflammatory cytokines in macrophages independent of nitric oxide formation, peroxisome proliferator-activated receptor-gamma activation, or induction of heme oxygenase-1 expression. The electrophilic nature of fatty acid nitroalkene derivatives resulted in alkylation of recombinant NF-kappa B p65 protein in vitro and a similar reaction with p65 in intact macrophages. The nitroalkylation of p65 by fatty acid nitroalkene derivatives inhibited DNA binding activity and repressed NF-kappa B-dependent target gene expression. Moreover, nitroalkenes inhibited endothelial tumor necrosis factor-alpha-induced vascular cell adhesion molecule 1 expression and monocyte rolling and adhesion. These observations indicate that nitroalkenes such as LNO2 and OA-NO2, derived from reactions of unsaturated fatty acids and oxides of nitrogen, are a class of endogenous anti-inflammatory mediators.
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