Glycyrrhizin affects monocyte migration and apoptosis by blocking HMGB1 signaling

Mol Med Rep. 2018 Apr;17(4):5970-5975. doi: 10.3892/mmr.2018.8598. Epub 2018 Feb 13.

Abstract

Monocytes serve an important role in systemic inflammation. High mobility group box‑1 protein (HMGB1) promotes recruitment and suppresses apoptosis in monocytes through the receptor for advanced glycation end products/ nuclear factor (NF)‑κB and toll‑like receptor 4/mitogen‑activated protein kinase (MAPK)/extracellular signal‑regulated kinase (ERK) signaling pathways. Glycyrrhizin (GL), an effective component of licorice, weakens the proinflammatory effect of HMGB1. The present study investigated the effect of GL on the migration and apoptosis of monocytes associated with HMGB1 signaling. THP‑1 cells were used to evaluate the behavior of monocytes in response to GL treatment, and the downstream pathways were investigated. GL suppressed HMGB1‑induced monocyte migration and increased HMGB1‑inhibited monocyte apoptosis. GL inhibited the activation of the NF‑κB and MAPK/ERK signaling pathways induced by HMGB1 and decreased the expression of monocyte chemoattractant protein‑1 (MCP‑1) and myeloid cell leukemia 1 (Mcl‑1). Taken together, the results indicated that GL may suppress the migration of monocytes and induce apoptosis to reduce systemic inflammation by blocking downstream NF‑κB/MCP‑1 and MAPK/ERK/Mcl‑1 signaling pathways.

Keywords: glycyrrhizin; monocyte; high mobility group box‑1 protein; receptor for advanced glycation end products; nuclear factor‑κB; toll‑like receptor 4; mitogen‑activated protein kinase; monocyte chemoattractant protein‑1; myeloid cell leukemia 1.

MeSH terms

  • Apoptosis / drug effects*
  • Cell Line
  • Cell Movement / drug effects
  • Chemokine CCL2 / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glycyrrhizic Acid / pharmacology*
  • HMGB1 Protein / metabolism*
  • Humans
  • Mitogen-Activated Protein Kinases / metabolism
  • Monocytes / drug effects*
  • Monocytes / immunology
  • Monocytes / metabolism*
  • NF-kappa B / metabolism
  • Signal Transduction / drug effects*

Substances

  • Chemokine CCL2
  • HMGB1 Protein
  • NF-kappa B
  • Glycyrrhizic Acid
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinases