4.7 Article

Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NIF-κB pathway

Journal

EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 761, Issue -, Pages 211-216

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2015.06.003

Keywords

Pinocembrin; LPS; NF-kappa B; PI3K; Microglia

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Pinocembrin, one of the primary flavonoids from Pirius heartwood and Eucalyptus, has been reported Lo have anti-inflammatory and antioxidant activity. This study was designed to evaluate the inhibitory effects of pinocembrin on inflammatory mediators production in LPS-stimulated BV2 microglial cells. The I esults showed that pinocembrin dose-dependently inhibited LPS-induced inflammatory mediators TNF-alpha, IL-1 beta, NO and PGE(2) production. Pinocembrin also inhibited LPS-induced iNOS and COX-2 expression. Moreover, pinocembrin inhibited LPS-induced PI3K, Akt phosphorylation, and NF-KE activation, which were required for inflammatory mediators production. Furthermore, treatment of pinocembrin induced nuclear translocation of Nrf2 and expression of HO-1. In conclusion, our data indicated that pinocembrin inhibited LPS-induced inflammatory mediators production by suppressing PI3K/Akt/NF-kappa B signaling pathway. (C) 2015 Elsevier B.V. All rights reserved.

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