Abstract
Neuroinflammation plays a critical role in the development of neurodegenerative diseases. Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been reported to have anti-inflammatory effect. The aim of this study was to investigate the anti-inflammatory effects and mechanism of taraxasterol in LPS-stimulated BV2 microglia cells. BV2 microglia cells were treated with taraxasterol 12 h before LPS stimulation. The effects of taraxasterol on LPS-induced TNF-α and IL-1β production were detected by ELISA. The effects of taraxasterol on LXRα, ABCA1, TLR4, and NF-κB expression were detected by western blot analysis. The results showed that taraxasterol dose-dependently inhibited LPS-induced TNF-α and IL-1β production and NF-κB activation. Taraxasterol also disrupted the formation of lipid rafts and inhibited translocation of TLR4 into lipid rafts. Furthermore, taraxasterol was found to activate LXRα-ABCA1 signaling pathway which induces cholesterol efflux from cells. In addition, our results showed that the anti-inflammatory effect of taraxasterol was attenuated by transfection with LXRα siRNA. In conclusion, these results suggested that taraxasterol inhibits LPS-induced inflammatory response in BV2 microglia cells by activating LXRα-ABCA1 signaling pathway.
Highlights
Neuroinflammation, a chronic inflammation in the brain, has been reported to play critical roles in the development of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease (Sun et al, 2010)
Our results showed that taraxasterol inhibited LPS-induced inflammatory response in BV2 microglia cells by activating LXRα-ABCA1 signaling pathway
The results showed that taraxasterol inhibited LPS-induced inflammatory cytokines production by activating LXRα-ABCA1 signaling pathway
Summary
Neuroinflammation, a chronic inflammation in the brain, has been reported to play critical roles in the development of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease (Sun et al, 2010). A type of primary immune cells in the brain, play critical roles in host defense and tissue repair in brain (Cameron and Landreth, 2010). Stimulation of microglia by LPS leads to the activation of TLR4 signaling pathway (Qin et al, 2005). The activation of TLR4 signaling pathway leads to the activation of NF-κB and release of inflammatory cytokines such as TNF-α and IL-1β (Kawai and Akira, 2007). TLR4 is the major receptor of LPS and inhibition of TLR4 signaling pathway could attenuate neurodegenerative diseases.
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