Scutellarin suppresses neuroinflammation via the inhibition of the AKT/NF-κB and p38/JNK pathway in LPS-induced BV-2 microglial cells

• DOI: 10.1007/s00210-018-1503-7
• Publication Date: 2018-04-21T01:29:42Z
• Authors: Pengtao You; San Fu; Kun Yu; Yu Xia; Hezhen Wu; Yanfang Yang; Chaozhi Ma; Dan Liu; Xin Chen; Jun Wang; Xiaochuan Ye; Yanwen Liu
• Keywords: Scutellarin; IκBα; IκB kinase

In 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.