Inhibitory effect of ferulic acid on macrophage inflammatory protein-2 production in a murine macrophage cell line, RAW264.7

Cytokine. 1997 Apr;9(4):242-8. doi: 10.1006/cyto.1996.0160.

Abstract

We investigated time-related productions of certain cytokines in lipopolysaccharide (LPS)-stimulated RAW264.7 cells, a murine macrophage cell line, by enzyme-linked immunosorbent assay. Macrophage inflammatory protein-2 (MIP-2) levels became detectable after 2 h and markedly increased over the first 8 h. Thereafter, this level remained at the same level between 10 and 16 h, and then increased again until 24 h, showing a tendency of biphasic pattern. Tumour necrosis factor (TNF)-alpha was detectable at 2 h and then increased sharply until 6 h at which it attained its peak. A low but recognizable level of interleukin (IL)-1alpha/beta was also detectable. When the inhibitory effect of ferulic acid (FA), an active component of the Rhizoma of Cimicifuga sp. used frequently as anti-inflammatory drug in Japanese Oriental medicines, was compared with that of dexamethasone (DX) on MIP-2 and TNF-alpha productions in response to LPS, both FA and DX could reduce the production of these cytokines in a dose-dependent manner. Concerning TNF-alpha, however, the inhibitory effect of FA was very weak compared with that of DX. In addition, FA as well as DX reduced MIP-2 production induced by TNF-alpha. These data suggest that MIP-2 might be induced by a direct effect of LPS and in part indirect one via initial induction of other cytokines such as TNF-alpha, leading a tendency of biphasic pattern. Comparing DX, FA is considered to be a novel and unique drug inhibiting MIP-2 production more selectively.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Chemokine CXCL2
  • Coumaric Acids / pharmacology*
  • Dexamethasone / pharmacology
  • Kinetics
  • Lipopolysaccharides / pharmacology
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Mice
  • Monokines / antagonists & inhibitors*
  • Monokines / biosynthesis*
  • Monokines / metabolism
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Chemokine CXCL2
  • Coumaric Acids
  • Lipopolysaccharides
  • Monokines
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • ferulic acid