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Anti-Inflammatory Effects of Sinapic Acid through the Suppression of Inducible Nitric Oxide Synthase, Cyclooxygase-2, and Proinflammatory Cytokines Expressions via Nuclear Factor-κB Inactivation

2008; American Chemical Society; Volume: 56; Issue: 21 Linguagem: Inglês

10.1021/jf802095g

1520-5118

Kyung-Jin Yun, Duck-Jae Koh, Shi-Hye Kim, Seung Jae Park, Jong Hoon Ryu, Deog-Gon Kim, Jin-Yong Lee, Kyung‐Tae Lee,

Immune Response and Inflammation

To investigate the anti-inflammatory potential of sinapic acid as well as the underlying mechanism involved, we studied the inhibitory effect of sinapic acid on the production of pro-inflammatory mediators in vitro and then evaluated its in vivo anti-inflammatory effect. Sinapic acid inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β production in a dose-dependent manner. Consistent with these findings, sinapic acid inhibited LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygase (COX)-2 at the protein levels, and iNOS, COX-2, TNF-α, and IL-1β mRNA expression in RAW 264.7 macrophages, as determined by Western blotting and reverse-transcribed polymerase chain reaction, respectively. Sinapic acid suppressed the LPS-induced activation of nuclear factor-κB (NF-κB), a transcription factor pivotal necessary for pro-inflammatory mediators, such as iNOS, COX-2, TNF-α, and IL-1β. This effect was accompanied by a parallel reduction of the nuclear translocation of p65 and p50 NF-κB subunits, as well as IκB-α degradation and phosphorylation. The effects of sinapic acid on acute phase inflammation were investigated on serotonin- and carrageenan-induced paw edema and compared with indomethacin (10 mg/kg, p.o.) or ibuprofen (100 mg/kg, p.o.). Maximum inhibitions of 34.2 and 44.5% were observed at a concentration of 30 mg/kg for serotonin- and carrageenan-induced paw edema, respectively. These results suggest that the suppressions of the expressions of iNOS, COX-2, TNF-α, and IL-1β via NF-κB inactivation are responsible for the anti-inflammatory effects of sinapic acid.