Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway

Alzheimer’s disease (AD) is a severe neurodegenerative disorder. AD is pathologically characterized by the formation of intracellular neurofibrillary tangles, and extracellular amyloid plaques which were comprised of amyloid-beta (Aβ) peptides. Aβ induces neurodegeneration by activating microglia, w...

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Autores principales: Buyun Kim, Ki Yong Lee, Byoungduck Park
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:4baf7a9168aa4bf180c7eed07365810e2021-11-25T18:29:30ZIsoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway10.3390/molecules262270561420-3049https://doaj.org/article/4baf7a9168aa4bf180c7eed07365810e2021-11-01T00:00:00Zhttps://www.mdpi.com/1420-3049/26/22/7056https://doaj.org/toc/1420-3049Alzheimer’s disease (AD) is a severe neurodegenerative disorder. AD is pathologically characterized by the formation of intracellular neurofibrillary tangles, and extracellular amyloid plaques which were comprised of amyloid-beta (Aβ) peptides. Aβ induces neurodegeneration by activating microglia, which triggers neurotoxicity by releasing various inflammatory mediators and reactive oxygen species (ROS). Nuclear factor-kappa B (NF-κB) is expressed in human tissues including the brain and plays an important role in Aβ-mediated neuronal inflammation. Thus, the identification of molecules that inhibit the NF-κB pathway is considered an attractive strategy for the treatment and prevention of AD. Isoorientin (3′,4′,5,7-Tetrahydroxy-6-C-glucopyranosyl flavone; ISO), which can be extracted from several plant species, such as <i>Philostachys</i> and <i>Patrinia</i> is known to have various pharmacological activities such as anticancer, antioxidant, and antibacterial activity. However, the effect of ISO on Aβ-mediated inflammation and apoptosis in the brain has yet to be elucidated. In the present study, we investigated whether ISO regulated Aβ-induced neuroinflammation in microglial cells and further explored the underlying mechanisms. Our results showed that ISO inhibited the expression of iNOS and COX-2 induced by Aβ<sub>25–35.</sub> And, it inhibited the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, ISO reduced the ROS production in Aβ<sub>25–35</sub>-induced BV2 cells and inhibited NF-κB activation. Furthermore, ISO blocked Aβ<sub>25–35</sub>-induced apoptosis of BV2 cells. Based on these findings, we suggest that ISO represents a promising therapeutic drug candidate for the treatment and prevention of AD.Buyun KimKi Yong LeeByoungduck ParkMDPI AGarticleAlzheimer’s diseaseamyloid-betaROSNF-κBinflammationOrganic chemistryQD241-441ENMolecules, Vol 26, Iss 7056, p 7056 (2021)
institution DOAJ
collection DOAJ
language EN
topic Alzheimer’s disease
amyloid-beta
ROS
NF-κB
inflammation
Organic chemistry
QD241-441
spellingShingle Alzheimer’s disease
amyloid-beta
ROS
NF-κB
inflammation
Organic chemistry
QD241-441
Buyun Kim
Ki Yong Lee
Byoungduck Park
Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
description Alzheimer’s disease (AD) is a severe neurodegenerative disorder. AD is pathologically characterized by the formation of intracellular neurofibrillary tangles, and extracellular amyloid plaques which were comprised of amyloid-beta (Aβ) peptides. Aβ induces neurodegeneration by activating microglia, which triggers neurotoxicity by releasing various inflammatory mediators and reactive oxygen species (ROS). Nuclear factor-kappa B (NF-κB) is expressed in human tissues including the brain and plays an important role in Aβ-mediated neuronal inflammation. Thus, the identification of molecules that inhibit the NF-κB pathway is considered an attractive strategy for the treatment and prevention of AD. Isoorientin (3′,4′,5,7-Tetrahydroxy-6-C-glucopyranosyl flavone; ISO), which can be extracted from several plant species, such as <i>Philostachys</i> and <i>Patrinia</i> is known to have various pharmacological activities such as anticancer, antioxidant, and antibacterial activity. However, the effect of ISO on Aβ-mediated inflammation and apoptosis in the brain has yet to be elucidated. In the present study, we investigated whether ISO regulated Aβ-induced neuroinflammation in microglial cells and further explored the underlying mechanisms. Our results showed that ISO inhibited the expression of iNOS and COX-2 induced by Aβ<sub>25–35.</sub> And, it inhibited the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, ISO reduced the ROS production in Aβ<sub>25–35</sub>-induced BV2 cells and inhibited NF-κB activation. Furthermore, ISO blocked Aβ<sub>25–35</sub>-induced apoptosis of BV2 cells. Based on these findings, we suggest that ISO represents a promising therapeutic drug candidate for the treatment and prevention of AD.
format article
author Buyun Kim
Ki Yong Lee
Byoungduck Park
author_facet Buyun Kim
Ki Yong Lee
Byoungduck Park
author_sort Buyun Kim
title Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
title_short Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
title_full Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
title_fullStr Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
title_full_unstemmed Isoorientin Inhibits Amyloid β<sub>25–35</sub>-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway
title_sort isoorientin inhibits amyloid β<sub>25–35</sub>-induced neuronal inflammation in bv2 cells by blocking the nf-κb signaling pathway
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/4baf7a9168aa4bf180c7eed07365810e
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AT kiyonglee isoorientininhibitsamyloidbsub2535subinducedneuronalinflammationinbv2cellsbyblockingthenfkbsignalingpathway
AT byoungduckpark isoorientininhibitsamyloidbsub2535subinducedneuronalinflammationinbv2cellsbyblockingthenfkbsignalingpathway
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