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Published on: July 25, 2022
Mangiferin inhibited neuroinflammation through regulating microglial polarization and suppressing NF-κB, NLRP3
Li-Yan Lei1, Rui-Cheng Wang2, Ya-Lei Pan1
1Shaanxi Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, Shaanxi Province Key Laboratory of New Drugs and Chinese Medicine Foundation Research, State Key Laboratory of Research & Development of Characteristic Qin Medicine Resources (Cultivation), Shaanxi University of Chinese Medicine, Xianyang 712083, China.
Abstract:
Inflammation plays important roles in the progress of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. Microglia is responsible for the homeostasis of the central nervous system (CNS), and involved in the neuroinflammation. Therefore, it could be potential in treatment of neurodegenerative diseases to suppress the microglia-mediated neuroinflammation. Mangiferin, a major glucoside of xanthone in Anemarrhena Rhizome, has anti-inflammatory, anti-diabetes, and anti-oxidative properties. However, the effect of mangiferin on the inflammatary responses of microglia cells are still poorly understand. In this study, we investigated the mechanism by which mangiferin inhibited inflammation in LPS-induced BV2 microglia cells. BV2 cells were pretreatment with mangiferin followed by LPS stimulation. In vitro assays, NO and cytokines production were quantified. Western blot and immunocytochemistry were used to examine the effect of mangiferin on the polarization of BV2 cells and signaling pathway. The results showed that mangiferin treatment significantly reduced NO, IL-1β, IL-6 and TNF-α production, also reduced the mRNA and protein of iNOS and COX-2, promoted the polarization of inflammatory toward anti-inflammatory, and inhibited activation of NF-κB and NLRP3 inflammasome. These data suggest that mangiferin has an anti-neuroinflammatory property via regulating microglia macrophage polarization and suppressing NF-κB and NLRP3 signaling pathway, and may act as a potential natural therapeutic candidate for neuroinflammatory diseases.
Insights
Mangiferin, a natural compound, effectively reduces neuroinflammation by modulating microglia activity and suppressing key inflammatory pathways. This suggests its potential as a therapeutic agent for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Neuroinflammation, driven by microglia, is crucial in neurodegenerative diseases like Parkinson's and Alzheimer's.
- Suppressing microglia-mediated neuroinflammation offers a potential therapeutic strategy for these conditions.
- Mangiferin, a xanthone glucoside, exhibits anti-inflammatory properties, but its effects on microglia remain unclear.
Purpose of the Study:
- To investigate the anti-neuroinflammatory mechanisms of mangiferin in lipopolysaccharide (LPS)-induced BV2 microglia cells.
- To determine mangiferin's impact on inflammatory responses, cell polarization, and signaling pathways in microglia.
Main Methods:
- BV2 microglia cells were pretreated with mangiferin before LPS stimulation.
- Assays quantified nitric oxide (NO) and cytokine production.
- Western blot and immunocytochemistry analyzed cell polarization and signaling pathway activation (NF-κB, NLRP3 inflammasome).
Main Results:
- Mangiferin significantly reduced NO, IL-1β, IL-6, and TNF-α production.
- It decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA and protein levels.
- Mangiferin promoted anti-inflammatory microglia polarization and inhibited NF-κB and NLRP3 inflammasome activation.
Conclusions:
- Mangiferin possesses anti-neuroinflammatory properties by regulating microglia polarization.
- It suppresses key inflammatory signaling pathways, including NF-κB and NLRP3 inflammasome.
- Mangiferin shows promise as a natural therapeutic candidate for neuroinflammatory diseases.
