Open Access

Effects of ganoderic acid A on lipopolysaccharide‑induced proinflammatory cytokine release from primary mouse microglia cultures

  • Authors:
    • Baojin Chi
    • Shuqiu Wang
    • Sheng Bi
    • Wenbo Qin
    • Dongmei Wu
    • Zhenguo Luo
    • Shiliang Gui
    • Dongwei Wang
    • Xingzhong Yin
    • Fangfang Wang
  • View Affiliations

  • Published online on: November 8, 2017     https://doi.org/10.3892/etm.2017.5472
  • Pages:847-853
  • Copyright: © Chi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

For several thousand years, Ganoderma lucidum (Ling‑Zhi in Chinese and Reishi in Japanese) has been widely used as a traditional medication for the prevention and treatment of various diseases in Asia. Its major biologically active components, ganoderic acids (GAs), exhibit significant medicinal value due to their anti‑inflammatory effects. Dysregulation of microglial function may cause seizures or promote epileptogenesis through release of proinflammatory cytokines, including interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α. At present, only little information is available on the effects of GAs on microglia‑mediated inflammation in vitro and/or in vivo. The present study aimed to investigate the role of GA‑A on microglia‑mediated inflammation in vitro. In addition, the effect of GA‑A on lipopolysaccharide (LPS)‑evoked alterations in mitochondrial metabolic activity of microglia was evaluated. The results of the present study demonstrated that GA‑A significantly decreased LPS‑induced IL‑1β, IL‑6 and TNF‑α release from mouse‑derived primary cortical microglial cells in a concentration‑dependent manner. GA‑A treatment reduced LPS‑induced expression of nuclear factor (NF)‑κB (p65) and its inhibitor, demonstrating that non‑toxic suppression of IL‑1β, IL‑6 and TNF‑α production by GA‑A is, at least in part, due to suppression of the NF‑κB signaling pathway. In addition, the LPS‑induced stimulation of mitochondrial activity of microglial cells was abolished by co‑treatment with GA‑A. Thus, GA‑A treatment may be a potential therapeutic strategy for epilepsy prevention by suppressing microglia‑derived proinflammatory mediators.

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January 2018
Volume 15 Issue 1

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

2016 Impact Factor: 1.261
Ranked #50/128 Medicine Research and Experimental
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APA
Chi, B., Wang, S., Bi, S., Qin, W., Wu, D., Luo, Z. ... Wang, F. (2018). Effects of ganoderic acid A on lipopolysaccharide‑induced proinflammatory cytokine release from primary mouse microglia cultures. Experimental and Therapeutic Medicine, 15, 847-853. https://doi.org/10.3892/etm.2017.5472
MLA
Chi, B., Wang, S., Bi, S., Qin, W., Wu, D., Luo, Z., Gui, S., Wang, D., Yin, X., Wang, F."Effects of ganoderic acid A on lipopolysaccharide‑induced proinflammatory cytokine release from primary mouse microglia cultures". Experimental and Therapeutic Medicine 15.1 (2018): 847-853.
Chicago
Chi, B., Wang, S., Bi, S., Qin, W., Wu, D., Luo, Z., Gui, S., Wang, D., Yin, X., Wang, F."Effects of ganoderic acid A on lipopolysaccharide‑induced proinflammatory cytokine release from primary mouse microglia cultures". Experimental and Therapeutic Medicine 15, no. 1 (2018): 847-853. https://doi.org/10.3892/etm.2017.5472