Abstract Title:

Baicalein inhibits TNF-α-induced NF-κB activation and expression of NF-κB-regulated target gene products.

Abstract Source:

Oncol Rep. 2016 Nov ;36(5):2771-2776. Epub 2016 Aug 19. PMID: 27667548

Abstract Author(s):

Junbo Li, Juan Ma, Ke Si Wang, Chunliu Mi, Zhe Wang, Lian Xun Piao, Guang Hua Xu, Xuezheng Li, Jung Joon Lee, Xuejun Jin

Article Affiliation:

Junbo Li


The nuclear factor-κB (NF-κB) transcription factors control many physiological processes including inflammation, immunity, apoptosis and angiogenesis. In our search for NF-κB inhibitors from natural resources, we identified baicalein from Scutellaria baicalensis as an inhibitor of NF-κB activation. As examined bythe NF-κB luciferase reporter assay, we found that baicalein suppressed TNF-α-induced NF-κB activation in a dose-dependent manner. It also inhibited TNF-α-induced nuclear translocation of p65 through inhibition of phosphorylation and degradation of IκBα. Furthermore, baicalein blocked the TNF-α-induced expression of NF-κB target genes involved in anti-apoptosis (cIAP-1, cIAP-2, FLIP and BCL-2), proliferation (COX-2, cyclin D1 and c-Myc), invasion (MMP‑9), angiogenesis (VEGF) and major inflammatory cytokines (IL-8 and MCP1). The flow cytometric analysis indicated that baicalein potentiated TNF-α-induced apoptosis and induced G1 phase arrest in HeLa cells. Moreover, baicalein significantly blocked activation of p38, extracellular signal-regulated kinase 1/2 (ERK1/2). Our results imply that baicalein could be a lead compound for the modulation of inflammatory diseases as well ascertain cancers in which inhibition of NF-κB activity may be desirable.

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