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A New Neolignan Derivative, Balanophonin Isolated from Firmiana simplex Delays the Progress of Neuronal Cell Death by Inhibiting Microglial Activation

Authors
Lim, Soo YoungSubedi, LalitaShin, DongyunKim, Chung SubLee, Kang RoKim, Sun Yeou
Issue Date
1-Sep-2017
Publisher
KOREAN SOC APPLIED PHARMACOLOGY
Keywords
Firmiana simplex; Neuroinflammation; Balanophonin; Microglia; Neuroprotection; Apoptosis
Citation
BIOMOLECULES & THERAPEUTICS, v.25, no.5, pp.519 - 527
Journal Title
BIOMOLECULES & THERAPEUTICS
Volume
25
Number
5
Start Page
519
End Page
527
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5722
DOI
10.4062/biomolther.2016.224
ISSN
1976-9148
Abstract
Excessive activation of microglia causes the continuous production of neurotoxic mediators, which further causes neuron degeneration. Therefore, inhibition of microglial activation is a possible target for the treatment of neurodegenerative disorders. Balanophonin, a natural neolignoid from Firmiana simplex, has been reported to have anti-inflammatory and anti-cancer effects. In this study, we aimed to evaluate the anti-neuroinflammatory effects and mechanism of balanophonin in lipopolysaccharide (LPS)stimulated BV2 microglia cells. BV2 microglia cells were stimulated with LPS in the presence or absence of balanophonin. The results indicated that balanophonin reduced not only the LPS-mediated TLR4 activation but also the production of inflammatory mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2), Interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha), in BV2 cells. Balanophonin also inhibited LPS-induced inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX2) protein. expression and mitogen activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 MAPK. Interestingly, it also inhibited neuronal cell death resulting from LPS-activated microglia by regulating cleaved caspase-3 and poly ADP ribose polymerase (PARP) cleavage in N2a cells. In conclusion, our data indicated that balanophonin may delay the progression of neuronal cell death by inhibiting microglial activation.
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