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

被引:71
|
作者
Zhou, Lu-ting [1 ]
Wang, Ke-jia [2 ]
Li, Ling [2 ]
Li, Hui [2 ]
Geng, Ming [1 ]
机构
[1] Gen Hosp Jinan Mil Command, Dept Pathol, Jinan 250031, Shandong, Peoples R China
[2] Second Mil Med Univ, Dept Pathophysiol, Shanghai 200433, Peoples R China
关键词
Pinocembrin; LPS; NF-kappa B; PI3K; Microglia; KAPPA-B ACTIVATION; ALZHEIMERS-DISEASE; ENDOTOXIC-SHOCK; UP-REGULATION; BRAIN; PROTECTS; NRF2; MECHANISM; TARGET; INJURY;
D O I
10.1016/j.ejphar.2015.06.003
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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.
引用
收藏
页码:211 / 216
页数:6
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