Selective inhibition of NF‐κB activation by the flavonoid hepatoprotector silymarin in HepG2
Claude SaliouDepartment of Molecular and Cell Biology, University of California, Berkeley 94720, USABertrand RihnLaboratoire de Toxicologie Expérimentale et Industrielle, Institut National de Recherche et de Sécurité, Avenue de Bourgogne, 54500 Vandoeuvre, FranceJosiane CillardLaboratoire de Biologie Cellulaire, Faculté de Pharmacie, 2, Avenue Pr. L. Bernard, Université de Rennes 1, 35043 Rennes, FranceTakashi OkamotoDepartment of Molecular Genetics, Nagoya City University, Medical School, Nagoya 467, JapanLester PackerDepartment of Molecular and Cell Biology, 251 Life Sciences Addition, University of California, Berkeley, CA 94720, USA
1998en
ABI
Аннотация
The bioflavonoid silymarin is found to potently suppress both nuclear factor kappa-B (NF-kappaB)-DNA binding activity and its dependent gene expression induced by okadaic acid in the hepatoma cell line HepG2. Surprisingly, tumor necrosis factor-alpha-induced NF-kappaB 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-kappaB, a key regulator in the inflammatory and immune reactions. Thus, the inhibitory effect of silymarin on NF-kappaB activation could be involved in its hepatoprotective property.
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