Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model
DC Field | Value | Language |
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dc.contributor.author | Sanjay | - |
dc.contributor.author | Shin, Jae-Ho | - |
dc.contributor.author | Park, Miey | - |
dc.contributor.author | Lee, Hae Jeung | - |
dc.date.accessioned | 2022-08-25T00:40:15Z | - |
dc.date.available | 2022-08-25T00:40:15Z | - |
dc.date.created | 2022-06-08 | - |
dc.date.issued | 2022-08 | - |
dc.identifier.issn | 0893-7648 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85283 | - |
dc.description.abstract | Microglial polarization plays an essential role in the progression and regression of neurodegenerative disorders. Cyanidin-3-O-glucoside (C3G), a dietary anthocyanin found in many fruits and vegetables, has been reported as an antioxidant, anti-inflammatory, and antitumor agent. However, there have been no reports on whether C3G can regulate the M1/M2 shift in an Alzheimer's disease model. We attempted to investigate the effects of C3G on M1/M2 polarization and the mechanism to regulate anti-inflammation and phagocytosis, both in vitro and in vivo. HMC3 cells were treated with beta-amyloid (A beta 42) in the presence or absence of 50 mu M C3G for different time intervals, and APPswe/PS1 Delta E9 mice were orally administered 30 mg/kg/day of C3G for 38 weeks. The in vitro data revealed that C3G could shift the M1 phenotype of microglia to M2 by reducing the expression of M1-specific markers (CD86 and CD80), inflammatory cytokines (IL-I beta, IL-6, TNF-alpha), reactive oxygen species, and enhancing the expression of M2-specific markers (CD206 and CD163). The APPswe/PS1 Delta E9 mice results were consistent with the in vitro data, indicating a significant reduction in inflammatory cytokines and higher expression of M2-specific markers such as CD206 and Arg1 in C3G-treated Alzheimer's disease model mice. Additionally, C3G was found to upregulate PPAR gamma expression levels both in vitro and in vivo, whereas a PPAR gamma antagonist (GW9662) was found to block C3G-mediated effects in vitro. In this study, we confirmed that C3G could regulate microglial polarization by activating PPAR gamma and eliminating accumulated beta-amyloid by enhancing A beta 42 phagocytosis through the upregulation of TREM2. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SPRINGER | - |
dc.relation.isPartOf | Molecular Neurobiology | - |
dc.title | Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000807327900003 | - |
dc.identifier.doi | 10.1007/s12035-022-02873-9 | - |
dc.identifier.bibliographicCitation | Molecular Neurobiology, v.59, no.8, pp.5135 - 5148 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85131504849 | - |
dc.citation.endPage | 5148 | - |
dc.citation.startPage | 5135 | - |
dc.citation.title | Molecular Neurobiology | - |
dc.citation.volume | 59 | - |
dc.citation.number | 8 | - |
dc.contributor.affiliatedAuthor | Sanjay | - |
dc.contributor.affiliatedAuthor | Park, Miey | - |
dc.contributor.affiliatedAuthor | Lee, Hae Jeung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | Neuroinflammation | - |
dc.subject.keywordAuthor | Anthocyanin | - |
dc.subject.keywordAuthor | Cyanidin-3-O-glucoside | - |
dc.subject.keywordAuthor | Anti-inflammation | - |
dc.subject.keywordAuthor | M1/M2 shift | - |
dc.subject.keywordPlus | PROLIFERATOR-ACTIVATED RECEPTOR | - |
dc.subject.keywordPlus | COGNITIVE IMPAIRMENT | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | ANTHOCYANINS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | ANTIOXIDANT | - |
dc.subject.keywordPlus | NEUROINFLAMMATION | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | PLASTICITY | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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