Ganoderma lucidum ethanol extract inhibits the inflammatory response by suppressing the NF-κB and toll-like receptor pathways in lipopolysaccharide-stimulated BV2 microglial cells

  • Authors:
    • Hyun-Min Yoon
    • Kyung-Jun Jang
    • Min Seok Han
    • Jin-Woo Jeong
    • Gi Young Kim
    • Jai-Heon Lee
    • Yung Hyun Choi
  • View Affiliations

  • Published online on: January 15, 2013     https://doi.org/10.3892/etm.2013.895
  • Pages: 957-963
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Ganoderma lucidum is a traditional Oriental medicine that has been widely used as a tonic to promote longevity and health in Korea and other Asian countries. Although a great deal of work has been carried out on the therapeutic potential of this mushroom, the pharmacological mechanisms of its anti-inflammatory actions remain unclear. In this study, we evaluated the inhibitory effects of G. lucidum ethanol extract (EGL) on the production of inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. We also investigated the effects of EGL on the LPS-induced activation of nuclear factor kappaB (NF-κB) and upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). Elevated levels of nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokine production were detected in BV2 microglia following LPS stimulation. We identifed that EGL significantly inhibits the excessive production of NO, PGE2 and pro-inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor-α in a concentration-dependent manner without causing cytotoxicity. In addition, EGL suppressed NF-κB translocation and transcriptional activity by blocking IκB degradation and inhibiting TLR4 and MyD88 expression in LPS-stimulated BV2 cells. Our results indicate that the inhibitory effects of EGL on LPS-stimulated inflammatory responses in BV2 microglia are associated with the suppression of the NF-κB and TLR signaling pathways. Therefore, EGL may be useful in the treatment of neurodegenerative diseases by inhibiting inflammatory mediator responses in activated microglia.
View Figures
View References

Related Articles

Journal Cover

March 2013
Volume 5 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yoon H, Jang K, Han MS, Jeong J, Kim GY, Lee J and Choi YH: Ganoderma lucidum ethanol extract inhibits the inflammatory response by suppressing the NF-κB and toll-like receptor pathways in lipopolysaccharide-stimulated BV2 microglial cells. Exp Ther Med 5: 957-963, 2013
APA
Yoon, H., Jang, K., Han, M.S., Jeong, J., Kim, G.Y., Lee, J., & Choi, Y.H. (2013). Ganoderma lucidum ethanol extract inhibits the inflammatory response by suppressing the NF-κB and toll-like receptor pathways in lipopolysaccharide-stimulated BV2 microglial cells. Experimental and Therapeutic Medicine, 5, 957-963. https://doi.org/10.3892/etm.2013.895
MLA
Yoon, H., Jang, K., Han, M. S., Jeong, J., Kim, G. Y., Lee, J., Choi, Y. H."Ganoderma lucidum ethanol extract inhibits the inflammatory response by suppressing the NF-κB and toll-like receptor pathways in lipopolysaccharide-stimulated BV2 microglial cells". Experimental and Therapeutic Medicine 5.3 (2013): 957-963.
Chicago
Yoon, H., Jang, K., Han, M. S., Jeong, J., Kim, G. Y., Lee, J., Choi, Y. H."Ganoderma lucidum ethanol extract inhibits the inflammatory response by suppressing the NF-κB and toll-like receptor pathways in lipopolysaccharide-stimulated BV2 microglial cells". Experimental and Therapeutic Medicine 5, no. 3 (2013): 957-963. https://doi.org/10.3892/etm.2013.895