Selective inhibition of NF‐κB activation by the flavonoid hepatoprotector silymarin in HepG2

FEBS Letters

Packer, Lester²  Rihn, Bertrand¹  Saliou, Claude²  Cillard, Josiane³  Okamoto, Takashi⁴ 

[1] Laboratoire de Toxicologie Expérimentale et Industrielle, Institut National de Recherche et de Sécurité, Avenue de Bourgogne, 54500 Vandoeuvre, France;Department of Molecular and Cell Biology, 251 Life Sciences Addition, University of California, Berkeley, CA 94720, USA;Laboratoire de Biologie Cellulaire, Faculté de Pharmacie, 2, Avenue Pr. L. Bernard, Université de Rennes 1, 35043 Rennes, France;Department of Molecular Genetics, Nagoya City University, Medical School, Nagoya 467, Japan

关键词: Nuclear factor kappa-B;    Antioxidant;    Hepatocyte;    Flavonoid;    Silymarin;    Inflammation;    EMSA;    electrophoretic mobility shift assay;    IKK;    IκB kinase;    LPS;    lipopolysaccharide;    OA;    okadaic acid;    PMA;    phorbol myristate acetate;    TNFα;    tumor necrosis factor;   

DOI  :  10.1016/S0014-5793(98)01409-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The bioflavonoid silymarin is found to potently suppress both nuclear factor kappa-B (NF-κB)-DNA binding activity and its dependent gene expression induced by okadaic acid in the hepatoma cell line HepG2. Surprisingly, tumor necrosis factor-α-induced NF-κB activation was not affected by silymarin, thus demonstrating a pathway-dependent inhibition by silymarin. Many genes encoding the proteins of the hepatic acute phase response are under the control of the transcription factor NF-κB, a key regulator in the inflammatory and immune reactions. Thus, the inhibitory effect of silymarin on NF-κB activation could be involved in its hepatoprotective property.

【 授权许可】

Unknown