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Abstract Title:

Saikosaponin B2 Suppresses Inflammatory Responses Through IKK/IκBα/NF-κB Signaling Inactivation in LPS-Induced RAW 264.7 Macrophages.

Abstract Source:

Inflammation. 2019 Feb ;42(1):342-353. PMID: 30251218

Abstract Author(s):

Ji-Sun Shin, Ho-Taek Im, Kyung-Tae Lee

Article Affiliation:

Ji-Sun Shin

Abstract:

Bupleurum falcatum (Umbelliferae) have been widely used to treat inflammatory diseases as traditional medicines in East Asian region. Although saikosaponins are main bioactive molecules of B. falcatum, there is little information on bioactivity of saikosaponin B(SSB2). This study was conducted to assess the anti-inflammatory activities and the involved mechanisms of SSB2 in LPS-induced RAW 264.7 macrophages. SSB2 suppressed the releases of nitric oxide (NO), prostaglandin E(PGE), tumor necrosis factorα (TNF-α), interleukins (IL)-6, and IL-1β by suppressing mRNA levels of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β, and IL-6 in LPS-induced macrophages. SSB2 blocked LPS-induced DNA binding and nuclear factor kappa B (NF-κB) transcriptional activity by inhibiting nuclear translocation p65 and p50, inhibitory κBα (IκBα) degradation, and IκB kinase β (IKKβ) phosphorylation and activity. In IKKβ-overexpressing cells, SSB2 significantly suppressed IKKβ-dependent NF-κB transcriptional activity. Moreover, SSB2 reduced phosphorylation of p38 and extracellularsignal-regulated kinase1/2 (ERK1/2). SSB2 effectively inhibits LPS-induced pro-inflammatory mediator releases by interfering with IKKβ and IκBα activation, thus preventing NF-κB activation. Our data indicates that SSB2 could be a potential therapeutic application for inflammation-associated diseases.

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