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Anti-neuroinflammatory effect of aurantiamide acetate from the marinefungus Aspergillus sp. SF-5921: Inhibition of NF-κB and MAPK pathwaysin lipopolysaccharide-induced mouse BV2 microglial cells

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Title
Anti-neuroinflammatory effect of aurantiamide acetate from the marinefungus Aspergillus sp. SF-5921: Inhibition of NF-κB and MAPK pathwaysin lipopolysaccharide-induced mouse BV2 microglial cells
Authors
Yoon, Chi-Su
Kim, Dong-Cheol
Lee, Dong-Sung
Kim, Kyoung-Su
Ko, Wonmin
Sohn, Jae Hak
Yim, Joung Han
Kim, Youn-Chul
Oh, Hyuncheol
Subject
Immunology; Pharmacology & Pharmacy
Keywords
Aurantiamide acetate; Aspergillus sp; Marine fungus; BV2 microglial cells; Anti-neuroinflammation
Issue Date
2014
Citation
Yoon, Chi-Su., et al. 2014. Anti-neuroinflammatory effect of aurantiamide acetate from the marinefungus Aspergillus sp. SF-5921: Inhibition of NF-κB and MAPK pathwaysin lipopolysaccharide-induced mouse BV2 microglial cells. International Immunopharmacology, 23: 568-574.
Abstract
In the course of a search for anti-neuroinflammatory metabolites from marine fungi, aurantiamide acetate (1) was isolated from marine-derived Aspergillus sp. as an anti-neuroinflammatory component. Compound 1 dosedependently inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in BV2 microglial cells. It also attenuated inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and other pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). In a further study designed to elucidate the mechanism of its anti-neuroinflammatory effect, compound 1 was shown to block the activation of nuclear factor-kappa B (NF-κB) in lipopolysaccharide (LPS)-induced BV2 microglial cells by inhibiting the phosphorylation of the inhibitor kappa B-α (IκB)-α. In addition, compound 1 decreased the phosphorylation levels of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs). These results suggest that compound 1 has an anti-neuroinflammatory effect on LPS stimulation through its inhibition of the NF-κB, JNK and p38 pathways.
DOI
10.1016/j.intimp.2014.10.006
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