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Schisandrol B and Schisandrin B Inhibit TGFβ1-mediated NF-κB Activation via a Smad-independent Mechanism

Schisandrol B and Schisandrin B Inhibit TGFβ1-mediated NF-κB Activation via a Smad-independent Mechanism

Jung Nyeo Chun, Soonbum Park, Sanghoon Lee, Jae-Kyung Kim, Eun-Jung Park, MinJi Kang, Hye Kyung Kim, Jong Kwan Park, Insuk So, Ju-Hong Jeon

Oncotarget. 2017 Dec 14;9(3):3121-3130.

PMID: 29423034

Abstract:

Aberrant transforming growth factor β1 (TGFβ1) signaling plays a pathogenic role in the development of vascular fibrosis. We have reported that Schisandra chinensis fruit extract (SCE), which has been used as a traditional oriental medicine, suppresses TGFβ1-mediated phenotypes in vascular smooth muscle cells (VSMCs). However, it is still largely unknown about the pharmacologic effects of SCE on various TGFβ1 signaling components. In this study, we found that SCE attenuated TGFβ1-induced NF-κB activation and nuclear translocation in VSMCs. Among the five active ingredients of SCE that were examined, schisandrol B (SolB) and schisandrin B (SchB) most potently suppressed TGFβ1-mediated NF-κB activation. In addition, SolB and SchB effectively inhibited IKKα/β activation and IκBα phosphorylation in TGFβ1-treated VSMCs. The pharmacologic effects of SolB and SchB on NF-κB activation were independent of the Smad-mediated canonical pathway. Therefore, our study demonstrates that SCE and its active constituents SolB and SchB suppress TGFβ1-mediated NF-κB signaling pathway in a Smad-independent mechanism. Our results may help further investigations to develop novel multi-targeted therapeutic strategies that treat or prevent vascular fibrotic diseases.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP58546546-A	Schisandrol B		58546-54-6	Price

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