• Pengtao You, San Fu, Kun Yu, Yu Xia, Hezhen Wu, Yanfang Yang, Chaozhi Ma, Dan Liu, Xin Chen, Jun Wang, Xiaochuan Ye, and Yanwen Liu.
• Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, 1 HuangJia Hu Road West, Hongshan District, Wuhan, Hubei, 430065, People's Republic of China. tptyou@hbtcm.edu.cn.
• Naunyn Schmiedebergs Arch. Pharmacol. 2018 Jul 1; 391 (7): 743-751.

AbstractIn vitro and in vivo studies indicate that scutellarin (SCU) exerts anti-inflammatory effects in the central nervous system (CNS) and inhibits microglia activation. This study investigated the anti-neuroinflammation molecular mechanisms exerted by scutellarin in LPS-induced BV-2 cells. The results showed that production of TNF-α, IL-1β, IL-6, and NO and TNF-α, IL-1β, IL-6, and iNOS mRNA were inhibited by scutellarin, which was independent of cytotoxicity as assessed by a CCK8 assay. Western blot analysis indicated that NF-κB-p65 phosphorylation was suppressed by scutellarin via inhibition of IκB degradation and IKKβ activation, which coincided with blockage of nuclear translocation of NF-κB as shown by immunofluorescent staining. Consistent with the inhibition of NF-κB, scutellarin inhibited the phosphorylation of p38, JNK, and AKT without affecting phosphorylation of ERK1/2 or PI3K in LPS-induced BV-2 cells. Overall, the present study suggests that scutellarin inhibits the production of pro-inflammatory mediators via inhibition of the IKK-dependent NF-κB and p38/JNK signaling pathway, which inhibits microglia activation and exerts anti-inflammation, indicating its potential therapeutic effect for neurodegenerative and cerebrovascular diseases.

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