1-(5-bromo-2-hydroxy-4- methoxyphenyl) ethanone [SE1] suppresses pro-inflammatory responses by blocking NF-κB and MAPK signaling pathways in activated microglia

Himaya, S. W. A., Ryu, BoMi, Qian, Zhong-Ji, Li, Yong and Kim, Se-Kwon (2011) 1-(5-bromo-2-hydroxy-4- methoxyphenyl) ethanone [SE1] suppresses pro-inflammatory responses by blocking NF-κB and MAPK signaling pathways in activated microglia. European Journal of Pharmacology, 670 2-3: 608-616. doi:10.1016/j.ejphar.2011.09.013


Author Himaya, S. W. A.
Ryu, BoMi
Qian, Zhong-Ji
Li, Yong
Kim, Se-Kwon
Title 1-(5-bromo-2-hydroxy-4- methoxyphenyl) ethanone [SE1] suppresses pro-inflammatory responses by blocking NF-κB and MAPK signaling pathways in activated microglia
Journal name European Journal of Pharmacology   Check publisher's open access policy
ISSN 0014-2999
1879-0712
Publication date 2011-11-30
Sub-type Article (original research)
DOI 10.1016/j.ejphar.2011.09.013
Open Access Status Not yet assessed
Volume 670
Issue 2-3
Start page 608
End page 616
Total pages 9
Place of publication Amsterdam, Netherlands
Publisher Elsevier
Language eng
Abstract Unregulated activation of microglia is a key risk factor contributes to neurodegenerative diseases and suppression of this phenomenon is considered as a potential therapeutic target. The compound isolated from sea horse Hippocampus kuda Bleeler; 1-(5-bromo-2-hydroxy-4-methoxyphenyl)ethanone [SE1] was characterized for its ability in suppressing LPS mediated activation of murine BV-2 cells. Despite the presence of various active molecular groups in the structure, SE1 has not well explored for its biological activities. The outcome of this study clearly indicated that SE1 inhibited the production of inflammatory mediators; nitric oxide, prostaglandin E2 and pro-inflammatory cytokines. Furthermore, it inhibited the protein and gene expression levels of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, interleukin-1β and interleukin-6. The responsible signaling mechanisms leading to these inhibitions were identified as SE1 mediated blocking of phosphorylation of mitogen activate protein kinase (MAPK) molecules; C-jun-N-terminal kinase (JNK), p38 and nuclear translocation of nuclear factor-κB (NF-κB) p65 and p50 subunits. These results suggest that SE1 has the potential to be further developed as therapeutic against neuro-inflammation.
Keyword 1-(5-bromo-2-hydroxy-4-methoxyphenyl)ethanone
Microglia
Anti-inflammation
MAPK
NF-κB
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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Created: Mon, 23 Jan 2017, 10:26:50 EST by Himaya Siddhihalu Wickrama Hewage on behalf of Institute for Molecular Bioscience