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M9480164.TXT
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1994-08-09
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Document 0164
DOCN M9480164
TI Inhibition of NF-kappa B transcription factor by catechol derivatives.
DT 9410
AU Suzuki YJ; Packer L; Department of Molecular & Cell Biology, University
of California,; Berkeley 94720.
SO Biochem Mol Biol Int. 1994 Feb;32(2):299-305. Unique Identifier :
AIDSLINE MED/94290341
AB Therapeutic agents which target NF-kappa B transcription factor may be
useful in the management of AIDS, cancer and inflammation. Since
oxidative stress has been implicated in the signaling pathway, the use
of antioxidants to inhibit NF-kappa B activation has gained attention.
In the present study, we examined the effects of catechol derivatives,
nitecapone and OR-1246, which have been identified to possess potent
antioxidant properties, on NF-kappa B activation by monitoring its DNA
binding activity. Both nitecapone and OR-1246 (10-300 microM) inhibited
NF-kappa B activation induced by tumor necrosis factor-alpha in Jurkat T
(acute human leukemia) cells. Nitecapone was a better inhibitor than
OR-1246. The observed effects may, at least in part, be due to the
ability of the two compounds to directly inhibit DNA binding activity of
activated NF-kappa B. The inhibitory capability of OR-1246 on NF-kappa B
DNA binding does not appear to be a sole mechanism, as it did not
inhibit NF-kappa B activation induced by okadaic acid. Hence, catechol
derivatives inhibit NF-kappa B transcription factor through multiple
mechanisms, and nitecapone and OR-1246 may be useful as therapeutic
agents targeting NF-kappa B.
DE Antioxidants/*PHARMACOLOGY Base Sequence Catechol
Methyltransferase/ANTAGONISTS & INHIB Catechols/*PHARMACOLOGY
Comparative Study Ethers, Cyclic/PHARMACOLOGY Human Leukemia, T-Cell
Molecular Sequence Data NF-kappa B/*ANTAGONISTS & INHIB
Pentanones/*PHARMACOLOGY Support, Non-U.S. Gov't Support, U.S. Gov't,
P.H.S. Tumor Cells, Cultured JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).