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Int Immunopharmacol. 2014 Mar;19(1):88-93. doi: 10.1016/j.intimp.2014.01.004. Epub 2014 Jan 18.

Mycoepoxydiene inhibits activation of BV2 microglia stimulated by lipopolysaccharide through suppressing NF-κB, ERK 1/2 and toll-like receptor pathways.

Author information

  • 1Department of Nuclear Medicine & Minnan PET Center, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China.
  • 2State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
  • 3School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong, China.
  • 4Department of Nuclear Medicine & Minnan PET Center, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China. Electronic address: wuhua1025@163.com.
  • 5State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, China. Electronic address: cdyu@xmu.edu.cn.

Abstract

Mycoepoxydiene (MED) is a polyketide isolated from the marine fungal Diaporthe sp. HLY-1 associated with mangroves. Although MED has been shown to have various biological effects such as antimicrobial, anti-cancer, and anti-inflammatory activities, its activities and cellular mechanisms during microglial activation have yet to be elucidated. In the present study, we assessed the anti-inflammatory effect of MED on the production of inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. MED significantly inhibited LPS-induced production of pro-inflammatory mediators such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interferon-γ (INF-γ), and nitric oxide (NO), whereas it increased anti-inflammatory interleukin-10 (IL-10) and transforming growth factor-β1 (TGF-β1) production in BV2 microglia in a concentration-dependent manner without causing cytotoxicity. Moreover, MED suppressed NF-κB activation by blocking IkappaB-α (IκB-α) degradation and inhibited the phosphorylation of ERK 1/2 and toll-like receptor 4 (TLR4) expression, but had no effect on the phosphorylation of JNK, and p38. Our results demonstrate that the inhibitory and promotion effect of MED on LPS-stimulated inflammatory mediators and anti-inflammatory factor production in BV2 microglia is associated with the suppression of the NF-κB, ERK1/2 and TLR signaling pathways. Therefore, MED may have therapeutic potential for neurodegenerative diseases by inhibiting inflammatory mediators and enhancing anti-inflammatory factor production in activated microglia.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

Microglia; Mitogen-activated protein kinase; Mycoepoxydiene; NF-κB; Pro-inflammatory mediators; Toll-like receptor

PMID:
24447679
[PubMed - indexed for MEDLINE]
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