title: Tormentic acid reduces inflammation in BV-2 microglia by activating the liver X receptor alpha.
abstract: 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 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.
authors.affiliation: Department of Neurology, He Bei Provincial Chest Hospital, Shi Jiazhuang 050000, China.
authors.forename: A
authors.initials: A
authors.lastname: Ma
authors.affiliation: Department of Nephrology, He Bei Provincial Chest Hospital, Shi Jiazhuang 050000, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neurology, He Bei Provincial Chest Hospital, Shi Jiazhuang 050000, China. Electronic address: zhengjieshenggz@163.com.
authors.forename: Q
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000633:toxicity; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D004660:Encephalitis / Q000378:metabolism / Q000517:prevention & control*; D006801:Humans; D008070:Lipopolysaccharides; D000071518:Liver X Receptors; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D057093:Orphan Nuclear Receptors / Q000378:metabolism*; D014315:Triterpenes / Q000008:administration & dosage* / Q000633:toxicity
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D000071518:Liver X Receptors; C000605213:NR1H3 protein, human; D057093:Orphan Nuclear Receptors; D014315:Triterpenes; C007695:euscaphic acid
keywords: LPS; LXRα; NF-κB; PGE(2); microglia; tormentic acid