6-7-Dimethoxy-4-methylcoumarin suppresses pro-inflammatory mediator expression through inactivation of the NF-κB and MAPK pathways in LPS-induced RAW 264.7 cells

Authors

  • Kil-Nam Kim Jeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea
  • Hye-Won Yang School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea
  • Seok-Chun Ko School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea
  • Yeong-Jong Ko Jeju Biodiversity Research Institute, Jeju Technopark, Jeju 699-943, Republic of Korea
  • Eun-A Kim School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea
  • Seong Woon Roh Jeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea
  • Eun-Yi Ko School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea
  • Ginnae Ahn Department of Marine Bio-Food Sciences, Chonnam National University, Yeosu 550-749, Republic of Korea
  • Soo-Jin Heo Global Bioresources Research Center, Korea Institute of Ocean Science & Technology, Ansan 426-744, Republic of Korea
  • You-Jin Jeon School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea
  • Weon-Jong Yoon Jeju Biodiversity Research Institute, Jeju Technopark, Jeju 699-943, Republic of Korea
  • Chang-Gu Hyun LINC Agency, Jeju National University, Jeju 690-756, Republic of Korea
  • Daekyung Kim Jeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea

Keywords:

6,7-Dimethoxy-4-methylcoumarin (DMC), anti-inflammatory, RAW 264.7 cells, NF-kappaB, MAPKs

Abstract

In this study, we investigated the ability of 6,7-dimethoxy-4-methylcoumarin (DMC) to inhibit lipopolysaccharide (LPS)-induced expression of pro-inflammatory mediators in mouse macrophage (RAW 264.7) cells, and the molecular mechanism through which this inhibition occurred. Our results indicated that DMC downregulated LPS-induced nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, thereby reducing the production of NO and prostaglandin E2 (PGE2) in LPS-activated RAW 264.7 cells. Furthermore, DMC suppressed LPS-induced production of pro-inflammatory cytokines such as interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α. To elucidate the mechanism underlying the anti-inflammatory activity of DMC, we assessed its effects on the mitogen-activated protein kinase (MAPK) pathway and the activity and expression of nuclear transcription factor kappa-B (NF-κB). The experiments demonstrated that DMC inhibited LPS-induced phosphorylation of extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinase (JNK), and p38. In addition, it attenuated LPS-induced NF-κB activation via the inhibition of IκB-α phosphorylation. Taken together, these data suggest that DMC exerts its anti-inflammatory effects in RAW 264.7 cells through the inhibition of LPS-stimulated NF-κB and MAPK signaling, thereby downregulating the expression of pro-inflammatory mediators.

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Published

2014-07-21

How to Cite

Kim, K.-N., Yang, H.-W., Ko, S.-C., Ko, Y.-J., Kim, E.-A., Roh, S. W., … Kim, D. (2014). 6-7-Dimethoxy-4-methylcoumarin suppresses pro-inflammatory mediator expression through inactivation of the NF-κB and MAPK pathways in LPS-induced RAW 264.7 cells. EXCLI Journal, 13, 792–800. Retrieved from https://www.excli.de/index.php/excli/article/view/741

Issue

Vol. 13 (2014)

Section

Original articles

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