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

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

doi:10.3892/or.2016.5108

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

Authors:
- Junbo Li
- Juan Ma
- Ke Si Wang
- Chunliu Mi
- Zhe Wang
- Lian Xun Piao
- Guang Hua Xu
- Xuezheng Li
- Jung Joon Lee
- Xuejun Jin
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Affiliations: Key Laboratory of Natural Resources of Changbai Mountain and Functional Molecules, Ministry of Education, Molecular Cancer Research Center, College of Pharmacy, Yanbian University, Yanji, Jilin 133002, P.R. China
Published online on: September 19, 2016 https://doi.org/10.3892/or.2016.5108
Pages: 2771-2776

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Abstract

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 by the 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 as certain cancers in which inhibition of NF-κB activity may be desirable.

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