Glycyrrhizin inhibits interleukin-8 production and nuclear factor-kappaB activity in lung epithelial cells, but not through glucocorticoid receptors

J Pharmacol Sci. 2008 Mar;106(3):460-8. doi: 10.1254/jphs.fp0072378. Epub 2008 Mar 12.

Abstract

This study was designed to examine the glucocorticoid-like inhibitory effect of glycyrrhizin (GL) on interleukin (IL)-8 production in A549 lung epithelial cells. GL, as well as dexamethasone (DEX) inhibited both tumor necrosis factor (TNF)-alpha- and IL-1beta-induced IL-8 production, mRNA expression, and promoter activity in A549 cells. Both GL and DEX inhibited transactivation of nuclear factor (NF)-kappaB, without inhibiting translocation of the NF-kappaB p65 subunit to the nucleus. However, the effect of GL was insensitive to RU486, a GR antagonist, and to GR knockdown by siRNA. Furthermore, only GL inhibited DNA binding of p65 to the IL-8 promoter region. These findings indicated that GL had a glucocorticoid-like inhibitory effect on IL-8 production via a mechanism that differs from that of glucocorticoids.

MeSH terms

  • Active Transport, Cell Nucleus
  • Anti-Inflammatory Agents / pharmacology*
  • Cell Line, Tumor
  • DNA / metabolism
  • Epithelial Cells / drug effects
  • Glycyrrhizic Acid / pharmacology*
  • Humans
  • Interleukin-8 / biosynthesis*
  • Interleukin-8 / genetics
  • Lung
  • Promoter Regions, Genetic
  • Receptors, Glucocorticoid / drug effects*
  • Receptors, Glucocorticoid / physiology
  • Transcription Factor RelA / metabolism*

Substances

  • Anti-Inflammatory Agents
  • Interleukin-8
  • Receptors, Glucocorticoid
  • Transcription Factor RelA
  • Glycyrrhizic Acid
  • DNA