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Title 

Anti-neuroinflammatory effects of citreohybridonol involving TLR4-MyD88-mediated inhibition of NF-кB and MAPK signaling pathways in lipopolysaccharide-stimulated BV2 cells

Authors 

K H ChoD C KimC S YoonW M KoS J LeeJ H SohnJae-Hyuk JangJong Seog AhnY C KimH Oh

Publisher 

Elsevier

Issue Date 

2016

Citation 

Neurochemistry International, vol. 95, no. 0, pp. 55-62

Keywords 

Anti-neuroinflammationCitreohybridonolMarine-derived fungusMitogen-activated protein kinase (MAPK)Nuclear factor-kappa B (NF-κB)

Abstract 

In the course of searching for anti-neuroinflammatory metabolites from marine fungi, citreohybridonol was isolated from marine-derived fungal strain Toxicocladosporium sp. SF-5699. Citreohybridonol inhibited production of nitric oxide (NO) and prostaglandin E2 (PGE2) in BV2 cells stimulated by lipopolysaccharide (LPS). Citreohybridonol also suppressed the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and other pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the LPS-stimulated cells. In the further study, citreohybridonol disturbed nuclear translocation of nuclear factor-kappa B (NF-κB) in LPS-stimulated BV2 cells by inhibiting the phosphorylation of the inhibitor kappa B-α (IκB-α). Citreohybridonol also had inhibitory effect on the LPS-stimulated phosphorylation of p38 mitogen-activated protein kinase (MAPK). Finally, citreohybridonol suppressed the protein expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) in LPS-induced BV2 cells. These results suggest that citreohybridonol has anti-neuroinflammatory effect in LPS-stimulated BV2 cells by modulating TLR4-mediated several inflammatory pathways such as NF-κB and p38 MAPK pathways.

ISSN 

0197-0186

Link 

http://dx.doi.org/10.1016/j.neuint.2015.12.010

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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