Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model
- Authors
- Sanjay; Shin, Jae-Ho; Park, Miey; Lee, Hae Jeung
- Issue Date
- Aug-2022
- Publisher
- SPRINGER
- Keywords
- Alzheimer' s disease; Neuroinflammation; Anthocyanin; Cyanidin-3-O-glucoside; Anti-inflammation; M1/M2 shift
- Citation
- Molecular Neurobiology, v.59, no.8, pp.5135 - 5148
- Journal Title
- Molecular Neurobiology
- Volume
- 59
- Number
- 8
- Start Page
- 5135
- End Page
- 5148
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85283
- DOI
- 10.1007/s12035-022-02873-9
- ISSN
- 0893-7648
- 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.
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