Anti-inflammatory effect of caffeine by regulating NF-κB activation in murine macrophage

Abstract

Caffeine is white crystalline xanthine alkaloid and found in the seeds, the coffee plant and the leaves of the tea bush. In this study, we determined whether caffeine exerts anti-inflammatory effects on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 cells.

To examine the effects of caffeine on LPS-induced inflammation, RAW 264.7 cells were treated with various concentrations of caffeine in the presence or absence of LPS.

Our data showed that caffeine decreased the LPS-induced inflammatory mediator, nitric oxide (NO). Caffeine treatment also reduced the expression of pro-inflammatory genes inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin (IL)-3, IL-6 and IL-12, and decreased IL-6 secretion and phosphorylated p38MAPK expression in LPS-treated RAW264.7 cells. Caffeine inhibited the nuclear translocation of nuclear factor κB (NF-κB) via IκBα phosphorylation. In addition, caffeine inhibited LPS-induced NO production in zebrafish.

Caffeine may inhibit LPS-induced inflammatory responses in murine macrophage by regulating NF-κB activation and MAPK phosphorylation.