ArticleNeural plasticity2016
Gypenoside Attenuates β Amyloid-Induced Inflammation in N9 Microglial Cells via SOCS1 Signaling.
Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
- Targeting Microglial Phagocytosis for Alzheimer's Disease Management: Natural, Pharmacological, Nanoparticle, and Gene Therapy Approaches.CNS & neurological disorders drug targets · 2026Review
- Gaultheria leucocarpa inhibits Aβ fibrillization and enhances mitophagy-mediated degradation of pathogenic proteins.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury.Inflammation · 2025Article
- Microglial Modulation in Alzheimer's Disease: Central Players in Neuroinflammation and Pathogenesis.Current Alzheimer research · 2025Review
- Gypensapogenin I alleviates PANoptosis, ferroptosis, and oxidative stress in myocardial ischemic-reperfusion injury by targeting the NOX2/AMPK pathway.Frontiers in cell and developmental biology · 2025Article
- Targeting Microglia in Alzheimer's Disease: Pathogenesis and Potential Therapeutic Strategies.Biomolecules · 2024Review
- Role of Network Pharmacology in Prediction of Mechanism of Neuroprotective Compounds.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Herbal medicines in Alzheimer's disease and the involvement of gut microbiota.Frontiers in pharmacology · 2024Review
- Article
- Effects of Probiotics on Colitis-Induced Exacerbation of Alzheimer's Disease inInternational journal of molecular sciences · 2023Article
- Modulation of Inflammatory Mediators and Microglial Activation Through Physical Exercise in Alzheimer's and Parkinson's Diseases.Neurochemical research · 2022Review
- Gypensapogenin I Ameliorates Isoproterenol (ISO)-Induced Myocardial Damage through Regulating the TLR4/NF-κB/NLRP3 Pathway.Molecules (Basel, Switzerland) · 2022Article
- Article
- Network pharmacology analysis reveals neuroprotection of Gynostemma pentaphyllum (Thunb.) Makino in Alzheimer' disease.BMC complementary medicine and therapies · 2022Article
- Prebiotic properties of jiaogulan in the context of gut microbiome.Food science & nutrition · 2022Review
- Article
- Gypenoside-Induced Apoptosis via the PI3K/AKT/mTOR Signaling Pathway in Bladder Cancer.BioMed research international · 2022Article
- Differences in Immune-Related Genes Underlie Temporal and Regional Pathological Progression in 3xTg-AD Mice.Cells · 2022Article
- Key brain cell interactions and contributions to the pathogenesis of Alzheimer's disease.Frontiers in cell and developmental biology · 2022Review
- MicroRNA miR-27b-3p regulate microglial inflammation response and cell apoptosis by inhibiting A20 (TNF-α-induced protein 3).Bioengineered · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reducing β amyloid- (Aβ-) induced microglial activation is believed to be effective in treating Alzheimer's disease (AD). Microglia can be activated into classic activated state (M1 state) or alternative activated state (M2 state), and the former is harmful; in contrast, the latter is beneficial. Gypenoside (GP) is the major bioactive constituent of Gynostemma pentaphyllum, a traditional Chinese herb medicine. In this study, we hypothesized that GP attenuates Aβ-induced microglial activation by ameliorating microglial M1/M2 states, and the process may be mediated by suppressor of cell signaling protein 1 (SOCS1). In this study, we found that Aβ exposure increased the levels of microglial M1 markers, including iNOS expression, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 releases, and coadministration of GP reversed the increase of M1 markers and enhanced the levels of M2 markers, including arginase-1 (Arg-1) expression, IL-10, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF) releases in the Aβ-treated microglial cells. SOCS1-siRNA, however, significantly abolished the GP-induced effects on the levels of microglial M1 and M2 markers. These findings indicated that GP attenuates Aβ-induced microglial activation by ameliorating M1/M2 states, and the process may be mediated by SOCS1.
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