Polydatin inhibits LPS-induced inflammatory response in BV2 microglia by disrupting the formation of lipid rafts
| Autor: | Liang Wu, Shaocai Hao, Yourui Zou, Shengyu Sun, Zhanfeng Niu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Cell Survival Inflammatory response Immunology Anti-Inflammatory Agents Toxicology Cell Line 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Membrane Microdomains Glucosides Stilbenes Immunology and Allergy Animals Lipid raft Protein kinase B Neuroinflammation Pharmacology Dose-Response Relationship Drug NF-κB General Medicine Cell biology 030104 developmental biology chemistry Bv2 microglia 030220 oncology & carcinogenesis Microglia Inflammation Mediators Drugs Chinese Herbal |
| Zdroj: | Immunopharmacology and immunotoxicology. 43(2) |
| ISSN: | 1532-2513 |
| Popis: | 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.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.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.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. |
| Databáze: | OpenAIRE |
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