• A Ma, Y Wang, and Q Zhang.
• Department of Neurology, He Bei Provincial Chest Hospital, Shi Jiazhuang 050000, China.
• Neuroscience. 2015 Feb 26;287:9-14.

AbstractTormentic 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 1h before exposure to LPS. The expression of inducible nitric oxide synthase (iNOS), Cyclooxygenase-2 (COX-2), Nuclear factor κB (NF-κB) and liver X receptor alpha (LXRα) was detected by western blotting. The expression of cytokines Tumor necrosis factor-alpha (TNF-α) and interleukin 1beta (IL-1β) 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-α and IL-1β expression. Furthermore, TA could activate LXRα and inhibit LPS-induced NF-κB activation. Knowdown of LXRα 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 LXRα.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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