The Inhibitory Mechanisms of Psoralidin on Lipopolysaccharide (LPS)-induced Nitric Oxide Production in RAW264.7 Macrophages

• Main Authors: Lin, Shi-Shiuan, 林晞璿
• Other Authors: Liao, Jyh-Fei
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/r97hdb

碩士 === 國立陽明大學 === 藥理學研究所 === 97 === Psoralidin is a natural product isolated from Psoralea corylifolia L., a herbal plant that is used in traditional Chinese medicine. The present results showed that this compound concentration (10, 20 and 30 uM)-dependently inhibited LPS-induced NO production in RAW264.7 macrophages via interfering with the activation of NF-kB/IkB/IKK and PI3K/Akt pathways,but didn’t affect MAPKs pathways activations. Furthermore, psoralidin inhibited LPS-induced IRAK1 activation and TAK1 phosphorylation. Syk is an upstream regulator of TLR4 signaling. However, the detail mechanism of Syk regulated TLR4 signaling is unclear. In this study, syk inhibitor piceatannol inhibitsed LPS-induced NO production, NF-kB, PI3K/Akt pathway and IRAK1 activations, but didn’t affect IKK/IkB pathway activation. It appears some similar action mechanisms between psoralidin and piceatannol. Transfection of siRNA targeting IRAK1, didn’t affect LPS-induced IKK/IkB pathway. Therefore, the anti-inflammatory mechanisms of psoralidin might inhibit LPS-induced IRAK1, PI3K/Akt pathway and IKK/I�菣B pathway independently and subsequently suppressing NF-k�羠 activation and NO production in RAW264.7 macrophages.