Glycyrrhizin affects monocyte migration and apoptosis by blocking HMGB1 signaling.

Mol Med Rep

Department of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.

Published: April 2018

AI Article Synopsis

  • Monocytes play a key role in systemic inflammation, influenced by HMGB1, which promotes their migration and prevents cell death through various signaling pathways.
  • Glycyrrhizin (GL), a component of licorice, reduces the inflammatory effects of HMGB1 by inhibiting these pathways and promoting the apoptosis of monocytes.
  • The study found that GL blocked HMGB1-induced monocyte migration and encouraged apoptosis, suggesting it could be a potential treatment to mitigate systemic inflammation by targeting specific signaling pathways.

Article 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.

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Source
http://dx.doi.org/10.3892/mmr.2018.8598DOI Listing

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