Diphlorethohydroxycarmalol inhibits interleukin-6 production by regulating NF-κB, STAT5 and SOCS1 in lipopolysaccharide-stimulated RAW264.7 cells

Na Jin Kang, Sang Chul Han, Gyeoung Jin Kang, Dong Hwan Koo, Young Sang Koh, Jin Won Hyun, Nam Ho Lee, Mi Hee Ko, Hee Kyoung Kang, Eun Sook Yoo

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

Diphlorethohydroxycarmalol (DPHC) is a phlorotannin compound isolated from Ishige okamuarae, a brown alga. This study was conducted to investigate the anti-inflammatory effect and action mechanism of DPHC in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We found that DPHC strongly reduces the production of interleukin 6 (IL-6), but not that of tumor necrosis factor-alpha (TNF-α) induced by LPS. DPHC (12.5 and 100 μM) suppressed the phosphorylation and the nuclear translocation of NF-kappaB (NF-κB), a central signaling molecule in the inflammation process induced by LPS. The suppressor of cytokine signaling 1 (SOCS1) is a negative feedback regulator of Janus kinase (Jak)-signal transducer and activator of transcription (STAT) signaling. In this study, DPHC inhibited STAT5 expression and upregulated that of SOCS1 at a concentration of 100 μM. Furthermore, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) (a specific NF-κB inhibitor) and JI (a specific Jak2 inhibitor) reduced the production of IL-6, but not that of tumor necrosis factor-alpha (TNF-α) in LPS-stimulated RAW 264.7 macrophages. These findings demonstrate that DPHC inhibits IL-6 production via the downregulation of NF-κB and Jak2-STAT5 pathway and upregulation of SOCS1.

Original languageEnglish (US)
Pages (from-to)2141-2157
Number of pages17
JournalMarine Drugs
Volume13
Issue number4
DOIs
StatePublished - Apr 1 2015

Bibliographical note

Publisher Copyright:
© 2015 by the authors; licensee MDPI.

Keywords

  • Diphlorethohydroxycarmalol (DPHC)
  • IL-6
  • Inflammation
  • Jak-STAT
  • LPS
  • NF-κB
  • SOCS

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