Zhou Lu-Ting, Wang Ke-Jia, Li Ling, Li Hui, Geng Ming
Department of Pathology, General Hospital of Jinan Military Command, Jinan 250031, Shandong Province, China.
Department of Pathophysiology, Second Military Medical University, Shanghai 200433, China.
Eur J Pharmacol. 2015 Aug 15;761:211-6. doi: 10.1016/j.ejphar.2015.06.003. Epub 2015 Jun 3.
Pinocembrin, one of the primary flavonoids from Pinus heartwood and Eucalyptus, has been reported to 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 results showed that pinocembrin dose-dependently inhibited LPS-induced inflammatory mediators TNF-α, IL-1β, NO and PGE2 production. Pinocembrin also inhibited LPS-induced iNOS and COX-2 expression. Moreover, pinocembrin inhibited LPS-induced PI3K, Akt phosphorylation, and NF-κB 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-κB signaling pathway.
松属心材和桉属植物中的主要黄酮类化合物之一的白杨素，已被报道具有抗炎和抗氧化活性。本研究旨在评估白杨素对脂多糖（LPS）刺激的BV2小胶质细胞中炎症介质产生的抑制作用。结果表明，白杨素剂量依赖性地抑制LPS诱导的炎症介质肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、一氧化氮（NO）和前列腺素E2（PGE2）的产生。白杨素还抑制LPS诱导的诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）的表达。此外，白杨素抑制LPS诱导的磷脂酰肌醇-3激酶（PI3K）、蛋白激酶B（Akt）磷酸化以及核因子κB（NF-κB）激活，而这些是炎症介质产生所必需的。此外，白杨素处理诱导了核因子E2相关因子2（Nrf2）的核转位和血红素加氧酶-1（HO-1）的表达。总之，我们的数据表明，白杨素通过抑制PI3K/Akt/NF-κB信号通路来抑制LPS诱导的炎症介质产生。
