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

Oct 10, 2008Journal of agricultural and food chemistry

Sinapic acid reduces inflammation by blocking key enzymes and immune signals through turning off a inflammation-controlling protein

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Abstract

Sinapic acid inhibited paw edema by up to 44.5% at a concentration of 30 mg/kg.

Sinapic acid reduced the production of pro-inflammatory substances such as nitric oxide, prostaglandin E2, tumor necrosis factor-alpha, and interleukin-1beta in a dose-dependent manner.
The compound decreased the expression of inducible nitric oxide synthase and cyclooxygenase-2 at both protein and mRNA levels in macrophages.
Activation of the nuclear factor-kappaB pathway, which is crucial for the production of pro-inflammatory mediators, was suppressed by sinapic acid.
Sinapic acid was effective in reducing both serotonin- and carrageenan-induced inflammation in animal models.

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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 E 2 (PGE 2), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1beta 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-alpha, and IL-1beta 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-kappaB (NF-kappaB), a transcription factor pivotal necessary for pro-inflammatory mediators, such as iNOS, COX-2, TNF-alpha, and IL-1beta. This effect was accompanied by a parallel reduction of the nuclear translocation of p65 and p50 NF-kappaB subunits, as well as IkappaB-alpha 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-alpha, and IL-1beta via NF-kappaB inactivation are responsible for the anti-inflammatory effects of sinapic acid.

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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

Abstract

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