Journal
NEUROSCIENCE
Volume 287, Issue -, Pages 9-14Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2014.12.005
Keywords
microglia; tormentic acid; NF-kappa B; PGE(2); LPS; LXR alpha
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Tormentic acid (TA) has been reported to have anticancer, anti-inflammatory and anti-atherogenic properties. However, the effects of TA on neuroinflammation have not been reported. In this study, we investigated whether TA inhibited lipopolysaccharide (LPS)-induced inflammatory response in BV2 microglia cells. BV2 microglia cells were treated with TA for 1 h before exposure to LPS. The expression of inducible nitric oxide synthase (iNOS), Cyclooxygenase- 2 (COX-2), Nuclear factor kappa B (NF-kappa B) and liver X receptor alpha (LXR alpha) was detected by western blotting. The expression of cytokines Tumor necrosis factor-alpha (TNF-alpha) and interleukin 1beta (IL-1 beta) was detected by enzyme-linked immunosorbent assays (ELISA). Results showed that TA inhibited nitric oxide (NO), prostaglandin E2 (PGE2) production by inhibiting iNOS and COX-2 expression. TA also inhibited LPS-induced inflammatory cytokines TNF-alpha and IL-1 beta expression. Furthermore, TA could activate LXRa and inhibit LPS-induced NF-kappa B activation. Knowdown of LXRa reversed the anti-inflammatory effects of TA. In conclusion, our results indicate that TA exerts an anti-inflammatory effect on LPS-stimulated BV2 microglia cells by activating LXR alpha. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
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