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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
Other Titles
해양기원 Aspergillus sp. SF-5921 균주로부터 aurantiamide acetate의 항신경염증 효과
Authors
Yoon, Chi-Su
Oh, Hyuncheol
김윤철
Yim, Joung Han
Sohn, Jae Hak
Ko, Wonmin
Kim, Kyung Soo
이동성
Kim, Dong-Cheol
Keywords
Anti-neuroinflammation; Aspergillus sp.; Aurantiamide acetate; BV2 microglial cells; Marine fungus
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.
URI
http://repository.kopri.re.kr/handle/201206/7315
DOI
http://dx.doi.org/10.1016/j.intimp.2014.10.006
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