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Polydatin inhibits LPS-induced inflammatory response in BV2 microglia by disrupting the formation of lipid rafts
Shengyu Sun1, Yourui Zou1, Shaocai Hao1
1Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, China.
Objective:
Polydatin has been used in the treatment of various inflammatory diseases. However, its role in the regulation of neuroinflammation has not been reported. In this study, we designed to investigate the anti-inflammatory effects of polydatin in LPS-stimulated BV2 microglia cells.
Methods:
Inflammatory mediators TNF-α, IL-1β, NO, and PGE2 production were measured by ELISA. The protein of signaling pathways were detected by western blot analysis.
Results:
The results showed that polydatin significantly ameliorated the production of TNF-α, IL-1β, NO, and PGE2 up-regulated by LPS. Polydatin also blocked LPS-induced NF-κB activation. In addition, PI3K and AKT, the up-stream molecules of NF-κB signaling pathway, were inhibited by the treatment of polydatin. Also, we found the formation of lipid rafts was inhibited by polydatin through attenuating the cholesterol content. Finally, polydatin was found to increase the expression of ABCA1 and ABCG1.
Conclusion:
In conclusion, the results of the present study suggested that polydatin exhibited its anti-inflammatory effects in BV2 cells through disrupting lipid rafts, which subsequently inhibiting PI3K/AKT signaling pathway.
Insights
Polydatin reduces neuroinflammation by disrupting lipid rafts and inhibiting the PI3K/AKT pathway in microglia cells. This natural compound ameliorates inflammatory mediator production and NF-κB activation.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Polydatin is recognized for treating inflammatory diseases.
- Its specific role in neuroinflammation remains largely uninvestigated.
- Microglia activation is central to neuroinflammation.
Purpose of the Study:
- To investigate the anti-inflammatory effects of polydatin.
- To explore polydatin's mechanism in LPS-stimulated BV2 microglia cells.
Main Methods:
- Quantification of inflammatory mediators (TNF-α, IL-1β, NO, PGE2) via ELISA.
- Western blot analysis to detect signaling pathway proteins.
- Assessment of lipid raft formation and cholesterol content.
Main Results:
- Polydatin significantly decreased LPS-induced TNF-α, IL-1β, NO, and PGE2 production.
- Polydatin inhibited LPS-induced NF-κB activation by targeting the PI3K/AKT pathway.
- Polydatin disrupted lipid raft formation and increased ABCA1/ABCG1 expression.
Conclusions:
- Polydatin exerts anti-inflammatory effects in microglia.
- Disruption of lipid rafts and subsequent inhibition of the PI3K/AKT pathway mediate polydatin's action.
- Polydatin shows potential as a therapeutic agent for neuroinflammatory conditions.
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